Targeting PAR2-mediated inflammation in osteoarthritis: a comprehensive in vitro evaluation of oleocanthal’s potential as a functional food intervention for chondrocyte protection and anti-inflammatory effects
Osteoarthritis (OA) is a prevalent degenerative joint disease characterized by chronic inflammation and progressive cartilage degradation, ultimately leading to joint dysfunction and disability. Oleocanthal (OC), a bioactive phenolic compound derived from extra virgin olive oil, has garnered signifi...
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| Published in | BMC musculoskeletal disorders Vol. 25; no. 1; pp. 769 - 23 |
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| Main Authors | , , , , |
| Format | Journal Article |
| Language | English |
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England
BioMed Central Ltd
01.10.2024
BioMed Central BMC |
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| Online Access | Get full text |
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| Abstract | Osteoarthritis (OA) is a prevalent degenerative joint disease characterized by chronic inflammation and progressive cartilage degradation, ultimately leading to joint dysfunction and disability. Oleocanthal (OC), a bioactive phenolic compound derived from extra virgin olive oil, has garnered significant attention due to its potent anti-inflammatory properties, which are comparable to those of non-steroidal anti-inflammatory drugs (NSAIDs). This study pioneers the investigation into the effects of OC on the Protease-Activated Receptor-2 (PAR-2) mediated inflammatory pathway in OA, aiming to validate its efficacy as a functional food-based therapeutic intervention.
To simulate cartilage tissue in vitro, human bone marrow-derived mesenchymal stem cells (BMSCs) were differentiated into chondrocytes. An inflammatory OA-like environment was induced in these chondrocytes using lipopolysaccharide (LPS) to mimic the pathological conditions of OA. The therapeutic effects of OC were evaluated by treating these inflamed chondrocytes with various concentrations of OC. The study focused on assessing key inflammatory markers, catabolic enzymes, and mitochondrial function to elucidate the protective mechanisms of OC. Mitochondrial function, specifically mitochondrial membrane potential (ΔΨm), was assessed using Rhodamine 123 staining, a fluorescent dye that selectively accumulates in active mitochondria. The integrity of ΔΨm serves as an indicator of mitochondrial and bioenergetic function. Additionally, Western blotting was employed to analyze protein expression levels, while real-time polymerase chain reaction (RT-PCR) was used to quantify gene expression of inflammatory cytokines and catabolic enzymes. Flow cytometry was utilized to measure cell viability and apoptosis, providing a comprehensive evaluation of OC's therapeutic effects on chondrocytes.
The results demonstrated that OC significantly downregulated PAR-2 expression in a dose-dependent manner, leading to a substantial reduction in pro-inflammatory cytokines, including TNF-α, IL-1β, and MCP-1. Furthermore, OC attenuated the expression of catabolic markers such as SOX4 and ADAMTS5, which are critically involved in cartilage matrix degradation. Importantly, OC was found to preserve mitochondrial membrane potential (ΔΨm) in chondrocytes subjected to inflammatory stress, as evidenced by Rhodamine 123 staining, indicating a protective effect on cellular bioenergetics. Additionally, OC modulated the Receptor Activator of Nuclear Factor Kappa-Β Ligand (RANKL)/Receptor Activator of Nuclear Factor Kappa-Β (RANK) pathway, suggesting a broader therapeutic action against the multifactorial pathogenesis of OA.
This study is the first to elucidate the modulatory effects of OC on the PAR-2 mediated inflammatory pathway in OA, revealing its potential as a multifaceted therapeutic agent that not only mitigates inflammation but also protects cartilage integrity. The preservation of mitochondrial function and modulation of the RANKL/RANK pathway further underscores OC's comprehensive therapeutic potential in counteracting the complex pathogenesis of OA. These findings position OC as a promising candidate for integration into nutritional interventions aimed at managing OA. However, further research is warranted to fully explore OC's therapeutic potential across different stages of OA and its long-term effects in musculoskeletal disorders. |
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| AbstractList | Abstract Background Osteoarthritis (OA) is a prevalent degenerative joint disease characterized by chronic inflammation and progressive cartilage degradation, ultimately leading to joint dysfunction and disability. Oleocanthal (OC), a bioactive phenolic compound derived from extra virgin olive oil, has garnered significant attention due to its potent anti-inflammatory properties, which are comparable to those of non-steroidal anti-inflammatory drugs (NSAIDs). This study pioneers the investigation into the effects of OC on the Protease-Activated Receptor-2 (PAR-2) mediated inflammatory pathway in OA, aiming to validate its efficacy as a functional food-based therapeutic intervention. Methods To simulate cartilage tissue in vitro, human bone marrow-derived mesenchymal stem cells (BMSCs) were differentiated into chondrocytes. An inflammatory OA-like environment was induced in these chondrocytes using lipopolysaccharide (LPS) to mimic the pathological conditions of OA. The therapeutic effects of OC were evaluated by treating these inflamed chondrocytes with various concentrations of OC. The study focused on assessing key inflammatory markers, catabolic enzymes, and mitochondrial function to elucidate the protective mechanisms of OC. Mitochondrial function, specifically mitochondrial membrane potential (ΔΨm), was assessed using Rhodamine 123 staining, a fluorescent dye that selectively accumulates in active mitochondria. The integrity of ΔΨm serves as an indicator of mitochondrial and bioenergetic function. Additionally, Western blotting was employed to analyze protein expression levels, while real-time polymerase chain reaction (RT-PCR) was used to quantify gene expression of inflammatory cytokines and catabolic enzymes. Flow cytometry was utilized to measure cell viability and apoptosis, providing a comprehensive evaluation of OC’s therapeutic effects on chondrocytes. Results The results demonstrated that OC significantly downregulated PAR-2 expression in a dose-dependent manner, leading to a substantial reduction in pro-inflammatory cytokines, including TNF-α, IL-1β, and MCP-1. Furthermore, OC attenuated the expression of catabolic markers such as SOX4 and ADAMTS5, which are critically involved in cartilage matrix degradation. Importantly, OC was found to preserve mitochondrial membrane potential (ΔΨm) in chondrocytes subjected to inflammatory stress, as evidenced by Rhodamine 123 staining, indicating a protective effect on cellular bioenergetics. Additionally, OC modulated the Receptor Activator of Nuclear Factor Kappa-Β Ligand (RANKL)/Receptor Activator of Nuclear Factor Kappa-Β (RANK) pathway, suggesting a broader therapeutic action against the multifactorial pathogenesis of OA. Conclusions This study is the first to elucidate the modulatory effects of OC on the PAR-2 mediated inflammatory pathway in OA, revealing its potential as a multifaceted therapeutic agent that not only mitigates inflammation but also protects cartilage integrity. The preservation of mitochondrial function and modulation of the RANKL/RANK pathway further underscores OC’s comprehensive therapeutic potential in counteracting the complex pathogenesis of OA. These findings position OC as a promising candidate for integration into nutritional interventions aimed at managing OA. However, further research is warranted to fully explore OC’s therapeutic potential across different stages of OA and its long-term effects in musculoskeletal disorders. Background Osteoarthritis (OA) is a prevalent degenerative joint disease characterized by chronic inflammation and progressive cartilage degradation, ultimately leading to joint dysfunction and disability. Oleocanthal (OC), a bioactive phenolic compound derived from extra virgin olive oil, has garnered significant attention due to its potent anti-inflammatory properties, which are comparable to those of non-steroidal anti-inflammatory drugs (NSAIDs). This study pioneers the investigation into the effects of OC on the Protease-Activated Receptor-2 (PAR-2) mediated inflammatory pathway in OA, aiming to validate its efficacy as a functional food-based therapeutic intervention. Methods To simulate cartilage tissue in vitro, human bone marrow-derived mesenchymal stem cells (BMSCs) were differentiated into chondrocytes. An inflammatory OA-like environment was induced in these chondrocytes using lipopolysaccharide (LPS) to mimic the pathological conditions of OA. The therapeutic effects of OC were evaluated by treating these inflamed chondrocytes with various concentrations of OC. The study focused on assessing key inflammatory markers, catabolic enzymes, and mitochondrial function to elucidate the protective mechanisms of OC. Mitochondrial function, specifically mitochondrial membrane potential ([DELA]Ψm), was assessed using Rhodamine 123 staining, a fluorescent dye that selectively accumulates in active mitochondria. The integrity of [DELA]Ψm serves as an indicator of mitochondrial and bioenergetic function. Additionally, Western blotting was employed to analyze protein expression levels, while real-time polymerase chain reaction (RT-PCR) was used to quantify gene expression of inflammatory cytokines and catabolic enzymes. Flow cytometry was utilized to measure cell viability and apoptosis, providing a comprehensive evaluation of OC's therapeutic effects on chondrocytes. Results The results demonstrated that OC significantly downregulated PAR-2 expression in a dose-dependent manner, leading to a substantial reduction in pro-inflammatory cytokines, including TNF-[alpha], IL-1[beta], and MCP-1. Furthermore, OC attenuated the expression of catabolic markers such as SOX4 and ADAMTS5, which are critically involved in cartilage matrix degradation. Importantly, OC was found to preserve mitochondrial membrane potential ([DELA]Ψm) in chondrocytes subjected to inflammatory stress, as evidenced by Rhodamine 123 staining, indicating a protective effect on cellular bioenergetics. Additionally, OC modulated the Receptor Activator of Nuclear Factor Kappa-Î Ligand (RANKL)/Receptor Activator of Nuclear Factor Kappa-Î (RANK) pathway, suggesting a broader therapeutic action against the multifactorial pathogenesis of OA. Conclusions This study is the first to elucidate the modulatory effects of OC on the PAR-2 mediated inflammatory pathway in OA, revealing its potential as a multifaceted therapeutic agent that not only mitigates inflammation but also protects cartilage integrity. The preservation of mitochondrial function and modulation of the RANKL/RANK pathway further underscores OC's comprehensive therapeutic potential in counteracting the complex pathogenesis of OA. These findings position OC as a promising candidate for integration into nutritional interventions aimed at managing OA. However, further research is warranted to fully explore OC's therapeutic potential across different stages of OA and its long-term effects in musculoskeletal disorders. Keywords: Osteoarthritis, Protease-activated receptor 2 (PAR-2), Oleocanthal, Anti-inflammatory agents, Chondrocytes, In vitro techniques, Cartilage, Signal transduction, Phenols, Inflammation mediators, Extracellular matrix, Mitochondrial membrane potential BackgroundOsteoarthritis (OA) is a prevalent degenerative joint disease characterized by chronic inflammation and progressive cartilage degradation, ultimately leading to joint dysfunction and disability. Oleocanthal (OC), a bioactive phenolic compound derived from extra virgin olive oil, has garnered significant attention due to its potent anti-inflammatory properties, which are comparable to those of non-steroidal anti-inflammatory drugs (NSAIDs). This study pioneers the investigation into the effects of OC on the Protease-Activated Receptor-2 (PAR-2) mediated inflammatory pathway in OA, aiming to validate its efficacy as a functional food-based therapeutic intervention.MethodsTo simulate cartilage tissue in vitro, human bone marrow-derived mesenchymal stem cells (BMSCs) were differentiated into chondrocytes. An inflammatory OA-like environment was induced in these chondrocytes using lipopolysaccharide (LPS) to mimic the pathological conditions of OA. The therapeutic effects of OC were evaluated by treating these inflamed chondrocytes with various concentrations of OC. The study focused on assessing key inflammatory markers, catabolic enzymes, and mitochondrial function to elucidate the protective mechanisms of OC. Mitochondrial function, specifically mitochondrial membrane potential (ΔΨm), was assessed using Rhodamine 123 staining, a fluorescent dye that selectively accumulates in active mitochondria. The integrity of ΔΨm serves as an indicator of mitochondrial and bioenergetic function. Additionally, Western blotting was employed to analyze protein expression levels, while real-time polymerase chain reaction (RT-PCR) was used to quantify gene expression of inflammatory cytokines and catabolic enzymes. Flow cytometry was utilized to measure cell viability and apoptosis, providing a comprehensive evaluation of OC’s therapeutic effects on chondrocytes.ResultsThe results demonstrated that OC significantly downregulated PAR-2 expression in a dose-dependent manner, leading to a substantial reduction in pro-inflammatory cytokines, including TNF-α, IL-1β, and MCP-1. Furthermore, OC attenuated the expression of catabolic markers such as SOX4 and ADAMTS5, which are critically involved in cartilage matrix degradation. Importantly, OC was found to preserve mitochondrial membrane potential (ΔΨm) in chondrocytes subjected to inflammatory stress, as evidenced by Rhodamine 123 staining, indicating a protective effect on cellular bioenergetics. Additionally, OC modulated the Receptor Activator of Nuclear Factor Kappa-Β Ligand (RANKL)/Receptor Activator of Nuclear Factor Kappa-Β (RANK) pathway, suggesting a broader therapeutic action against the multifactorial pathogenesis of OA.ConclusionsThis study is the first to elucidate the modulatory effects of OC on the PAR-2 mediated inflammatory pathway in OA, revealing its potential as a multifaceted therapeutic agent that not only mitigates inflammation but also protects cartilage integrity. The preservation of mitochondrial function and modulation of the RANKL/RANK pathway further underscores OC’s comprehensive therapeutic potential in counteracting the complex pathogenesis of OA. These findings position OC as a promising candidate for integration into nutritional interventions aimed at managing OA. However, further research is warranted to fully explore OC’s therapeutic potential across different stages of OA and its long-term effects in musculoskeletal disorders. Osteoarthritis (OA) is a prevalent degenerative joint disease characterized by chronic inflammation and progressive cartilage degradation, ultimately leading to joint dysfunction and disability. Oleocanthal (OC), a bioactive phenolic compound derived from extra virgin olive oil, has garnered significant attention due to its potent anti-inflammatory properties, which are comparable to those of non-steroidal anti-inflammatory drugs (NSAIDs). This study pioneers the investigation into the effects of OC on the Protease-Activated Receptor-2 (PAR-2) mediated inflammatory pathway in OA, aiming to validate its efficacy as a functional food-based therapeutic intervention. To simulate cartilage tissue in vitro, human bone marrow-derived mesenchymal stem cells (BMSCs) were differentiated into chondrocytes. An inflammatory OA-like environment was induced in these chondrocytes using lipopolysaccharide (LPS) to mimic the pathological conditions of OA. The therapeutic effects of OC were evaluated by treating these inflamed chondrocytes with various concentrations of OC. The study focused on assessing key inflammatory markers, catabolic enzymes, and mitochondrial function to elucidate the protective mechanisms of OC. Mitochondrial function, specifically mitochondrial membrane potential (ΔΨm), was assessed using Rhodamine 123 staining, a fluorescent dye that selectively accumulates in active mitochondria. The integrity of ΔΨm serves as an indicator of mitochondrial and bioenergetic function. Additionally, Western blotting was employed to analyze protein expression levels, while real-time polymerase chain reaction (RT-PCR) was used to quantify gene expression of inflammatory cytokines and catabolic enzymes. Flow cytometry was utilized to measure cell viability and apoptosis, providing a comprehensive evaluation of OC's therapeutic effects on chondrocytes. The results demonstrated that OC significantly downregulated PAR-2 expression in a dose-dependent manner, leading to a substantial reduction in pro-inflammatory cytokines, including TNF-α, IL-1β, and MCP-1. Furthermore, OC attenuated the expression of catabolic markers such as SOX4 and ADAMTS5, which are critically involved in cartilage matrix degradation. Importantly, OC was found to preserve mitochondrial membrane potential (ΔΨm) in chondrocytes subjected to inflammatory stress, as evidenced by Rhodamine 123 staining, indicating a protective effect on cellular bioenergetics. Additionally, OC modulated the Receptor Activator of Nuclear Factor Kappa-Β Ligand (RANKL)/Receptor Activator of Nuclear Factor Kappa-Β (RANK) pathway, suggesting a broader therapeutic action against the multifactorial pathogenesis of OA. This study is the first to elucidate the modulatory effects of OC on the PAR-2 mediated inflammatory pathway in OA, revealing its potential as a multifaceted therapeutic agent that not only mitigates inflammation but also protects cartilage integrity. The preservation of mitochondrial function and modulation of the RANKL/RANK pathway further underscores OC's comprehensive therapeutic potential in counteracting the complex pathogenesis of OA. These findings position OC as a promising candidate for integration into nutritional interventions aimed at managing OA. However, further research is warranted to fully explore OC's therapeutic potential across different stages of OA and its long-term effects in musculoskeletal disorders. Osteoarthritis (OA) is a prevalent degenerative joint disease characterized by chronic inflammation and progressive cartilage degradation, ultimately leading to joint dysfunction and disability. Oleocanthal (OC), a bioactive phenolic compound derived from extra virgin olive oil, has garnered significant attention due to its potent anti-inflammatory properties, which are comparable to those of non-steroidal anti-inflammatory drugs (NSAIDs). This study pioneers the investigation into the effects of OC on the Protease-Activated Receptor-2 (PAR-2) mediated inflammatory pathway in OA, aiming to validate its efficacy as a functional food-based therapeutic intervention. To simulate cartilage tissue in vitro, human bone marrow-derived mesenchymal stem cells (BMSCs) were differentiated into chondrocytes. An inflammatory OA-like environment was induced in these chondrocytes using lipopolysaccharide (LPS) to mimic the pathological conditions of OA. The therapeutic effects of OC were evaluated by treating these inflamed chondrocytes with various concentrations of OC. The study focused on assessing key inflammatory markers, catabolic enzymes, and mitochondrial function to elucidate the protective mechanisms of OC. Mitochondrial function, specifically mitochondrial membrane potential ([DELA]Ψm), was assessed using Rhodamine 123 staining, a fluorescent dye that selectively accumulates in active mitochondria. The integrity of [DELA]Ψm serves as an indicator of mitochondrial and bioenergetic function. Additionally, Western blotting was employed to analyze protein expression levels, while real-time polymerase chain reaction (RT-PCR) was used to quantify gene expression of inflammatory cytokines and catabolic enzymes. Flow cytometry was utilized to measure cell viability and apoptosis, providing a comprehensive evaluation of OC's therapeutic effects on chondrocytes. The results demonstrated that OC significantly downregulated PAR-2 expression in a dose-dependent manner, leading to a substantial reduction in pro-inflammatory cytokines, including TNF-[alpha], IL-1[beta], and MCP-1. Furthermore, OC attenuated the expression of catabolic markers such as SOX4 and ADAMTS5, which are critically involved in cartilage matrix degradation. Importantly, OC was found to preserve mitochondrial membrane potential ([DELA]Ψm) in chondrocytes subjected to inflammatory stress, as evidenced by Rhodamine 123 staining, indicating a protective effect on cellular bioenergetics. Additionally, OC modulated the Receptor Activator of Nuclear Factor Kappa-Î Ligand (RANKL)/Receptor Activator of Nuclear Factor Kappa-Î (RANK) pathway, suggesting a broader therapeutic action against the multifactorial pathogenesis of OA. This study is the first to elucidate the modulatory effects of OC on the PAR-2 mediated inflammatory pathway in OA, revealing its potential as a multifaceted therapeutic agent that not only mitigates inflammation but also protects cartilage integrity. The preservation of mitochondrial function and modulation of the RANKL/RANK pathway further underscores OC's comprehensive therapeutic potential in counteracting the complex pathogenesis of OA. These findings position OC as a promising candidate for integration into nutritional interventions aimed at managing OA. However, further research is warranted to fully explore OC's therapeutic potential across different stages of OA and its long-term effects in musculoskeletal disorders. Osteoarthritis (OA) is a prevalent degenerative joint disease characterized by chronic inflammation and progressive cartilage degradation, ultimately leading to joint dysfunction and disability. Oleocanthal (OC), a bioactive phenolic compound derived from extra virgin olive oil, has garnered significant attention due to its potent anti-inflammatory properties, which are comparable to those of non-steroidal anti-inflammatory drugs (NSAIDs). This study pioneers the investigation into the effects of OC on the Protease-Activated Receptor-2 (PAR-2) mediated inflammatory pathway in OA, aiming to validate its efficacy as a functional food-based therapeutic intervention.BACKGROUNDOsteoarthritis (OA) is a prevalent degenerative joint disease characterized by chronic inflammation and progressive cartilage degradation, ultimately leading to joint dysfunction and disability. Oleocanthal (OC), a bioactive phenolic compound derived from extra virgin olive oil, has garnered significant attention due to its potent anti-inflammatory properties, which are comparable to those of non-steroidal anti-inflammatory drugs (NSAIDs). This study pioneers the investigation into the effects of OC on the Protease-Activated Receptor-2 (PAR-2) mediated inflammatory pathway in OA, aiming to validate its efficacy as a functional food-based therapeutic intervention.To simulate cartilage tissue in vitro, human bone marrow-derived mesenchymal stem cells (BMSCs) were differentiated into chondrocytes. An inflammatory OA-like environment was induced in these chondrocytes using lipopolysaccharide (LPS) to mimic the pathological conditions of OA. The therapeutic effects of OC were evaluated by treating these inflamed chondrocytes with various concentrations of OC. The study focused on assessing key inflammatory markers, catabolic enzymes, and mitochondrial function to elucidate the protective mechanisms of OC. Mitochondrial function, specifically mitochondrial membrane potential (ΔΨm), was assessed using Rhodamine 123 staining, a fluorescent dye that selectively accumulates in active mitochondria. The integrity of ΔΨm serves as an indicator of mitochondrial and bioenergetic function. Additionally, Western blotting was employed to analyze protein expression levels, while real-time polymerase chain reaction (RT-PCR) was used to quantify gene expression of inflammatory cytokines and catabolic enzymes. Flow cytometry was utilized to measure cell viability and apoptosis, providing a comprehensive evaluation of OC's therapeutic effects on chondrocytes.METHODSTo simulate cartilage tissue in vitro, human bone marrow-derived mesenchymal stem cells (BMSCs) were differentiated into chondrocytes. An inflammatory OA-like environment was induced in these chondrocytes using lipopolysaccharide (LPS) to mimic the pathological conditions of OA. The therapeutic effects of OC were evaluated by treating these inflamed chondrocytes with various concentrations of OC. The study focused on assessing key inflammatory markers, catabolic enzymes, and mitochondrial function to elucidate the protective mechanisms of OC. Mitochondrial function, specifically mitochondrial membrane potential (ΔΨm), was assessed using Rhodamine 123 staining, a fluorescent dye that selectively accumulates in active mitochondria. The integrity of ΔΨm serves as an indicator of mitochondrial and bioenergetic function. Additionally, Western blotting was employed to analyze protein expression levels, while real-time polymerase chain reaction (RT-PCR) was used to quantify gene expression of inflammatory cytokines and catabolic enzymes. Flow cytometry was utilized to measure cell viability and apoptosis, providing a comprehensive evaluation of OC's therapeutic effects on chondrocytes.The results demonstrated that OC significantly downregulated PAR-2 expression in a dose-dependent manner, leading to a substantial reduction in pro-inflammatory cytokines, including TNF-α, IL-1β, and MCP-1. Furthermore, OC attenuated the expression of catabolic markers such as SOX4 and ADAMTS5, which are critically involved in cartilage matrix degradation. Importantly, OC was found to preserve mitochondrial membrane potential (ΔΨm) in chondrocytes subjected to inflammatory stress, as evidenced by Rhodamine 123 staining, indicating a protective effect on cellular bioenergetics. Additionally, OC modulated the Receptor Activator of Nuclear Factor Kappa-Β Ligand (RANKL)/Receptor Activator of Nuclear Factor Kappa-Β (RANK) pathway, suggesting a broader therapeutic action against the multifactorial pathogenesis of OA.RESULTSThe results demonstrated that OC significantly downregulated PAR-2 expression in a dose-dependent manner, leading to a substantial reduction in pro-inflammatory cytokines, including TNF-α, IL-1β, and MCP-1. Furthermore, OC attenuated the expression of catabolic markers such as SOX4 and ADAMTS5, which are critically involved in cartilage matrix degradation. Importantly, OC was found to preserve mitochondrial membrane potential (ΔΨm) in chondrocytes subjected to inflammatory stress, as evidenced by Rhodamine 123 staining, indicating a protective effect on cellular bioenergetics. Additionally, OC modulated the Receptor Activator of Nuclear Factor Kappa-Β Ligand (RANKL)/Receptor Activator of Nuclear Factor Kappa-Β (RANK) pathway, suggesting a broader therapeutic action against the multifactorial pathogenesis of OA.This study is the first to elucidate the modulatory effects of OC on the PAR-2 mediated inflammatory pathway in OA, revealing its potential as a multifaceted therapeutic agent that not only mitigates inflammation but also protects cartilage integrity. The preservation of mitochondrial function and modulation of the RANKL/RANK pathway further underscores OC's comprehensive therapeutic potential in counteracting the complex pathogenesis of OA. These findings position OC as a promising candidate for integration into nutritional interventions aimed at managing OA. However, further research is warranted to fully explore OC's therapeutic potential across different stages of OA and its long-term effects in musculoskeletal disorders.CONCLUSIONSThis study is the first to elucidate the modulatory effects of OC on the PAR-2 mediated inflammatory pathway in OA, revealing its potential as a multifaceted therapeutic agent that not only mitigates inflammation but also protects cartilage integrity. The preservation of mitochondrial function and modulation of the RANKL/RANK pathway further underscores OC's comprehensive therapeutic potential in counteracting the complex pathogenesis of OA. These findings position OC as a promising candidate for integration into nutritional interventions aimed at managing OA. However, further research is warranted to fully explore OC's therapeutic potential across different stages of OA and its long-term effects in musculoskeletal disorders. |
| ArticleNumber | 769 |
| Audience | Academic |
| Author | Varghese, Riah Banerjee, Yajnavalka Jannati, Shirin Naidoo, Nerissa Patnaik, Rajashree |
| Author_xml | – sequence: 1 givenname: Rajashree surname: Patnaik fullname: Patnaik, Rajashree – sequence: 2 givenname: Riah surname: Varghese fullname: Varghese, Riah – sequence: 3 givenname: Shirin surname: Jannati fullname: Jannati, Shirin – sequence: 4 givenname: Nerissa surname: Naidoo fullname: Naidoo, Nerissa – sequence: 5 givenname: Yajnavalka surname: Banerjee fullname: Banerjee, Yajnavalka |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/39354427$$D View this record in MEDLINE/PubMed |
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| CitedBy_id | crossref_primary_10_3390_ijms26072934 |
| Cites_doi | 10.1016/j.clim.2006.08.004 10.3389/fmolb.2021.703110 10.1371/journal.pone.0290739 10.1136/ard.2010.130336 10.3389/fimmu.2019.01412 10.1084/jem.20191430 10.3727/096368916X693464 10.1186/1423-0127-18-43 10.1172/JCI105945 10.1038/s41598-021-03346-0 10.1016/j.bone.2009.02.015 10.1101/gr.3.3.S30 10.1073/pnas.91.9.3652 10.3389/fimmu.2022.789349 10.1155/2021/5558066 10.1080/10408398.2019.1650715 10.1186/s12891-022-05949-8 10.3389/fendo.2018.00257 10.1016/j.cyto.2022.155805 10.1186/ar3657 10.3390/ijms22179208 10.1016/j.joca.2005.07.018 10.1016/j.clnu.2018.11.032 10.1016/j.joca.2010.07.003 10.1136/annrheumdis-2014-205779 10.1002/art.24255 10.1016/S1369-5274(99)00046-6 10.1016/j.tibtech.2012.12.003 10.1016/j.lfs.2012.09.012 10.1111/wrr.13137 10.18632/aging.102586 10.1080/10408390701429526 10.3389/fphar.2022.999851 10.1016/j.joca.2021.09.012 10.1172/JCI115950 10.3390/nu9101060 10.1002/art.20867 10.3892/etm.2023.12180 10.1016/j.joca.2008.05.009 10.3390/ijms22147645 10.3390/biology12081061 10.1152/physrev.00026.2013 10.1096/fj.201700265R 10.3390/metabo10100392 10.3390/antiox12122112 10.1038/437045a 10.1016/j.joca.2006.04.015 10.1096/fj.201800259R 10.1186/1471-2474-13-154 10.1038/s41467-018-06187-0 10.1177/19476035211063858 10.1016/S0022-2836(05)80360-2 10.1002/art.27476 10.4103/aca.ACA_94_19 10.1016/j.ebiom.2019.02.035 10.1038/nrrheum.2010.213 10.1006/meth.2001.1262 10.1016/j.clnu.2016.09.035 10.2196/42964 10.1093/ecam/nem132 10.1083/jcb.88.3.526 10.3390/antiox10050650 10.1172/JCI16913 10.1002/jor.23471 10.1186/s13098-023-01052-7 10.12997/jla.2023.12.2.89 10.1002/art.27437 10.1172/JCI119316 10.1016/j.smim.2014.05.004 10.3390/ijerph13080755 10.3390/ijms25168727 10.1016/j.exger.2021.111616 10.1056/NEJMoa1800389 10.1186/s13018-020-02045-2 10.7554/eLife.36163 10.1038/nrrheum.2013.135 10.3390/ijms17122042 10.1177/1947603518764262 10.1159/000493840 10.3390/medicina59020191 10.1038/nrrheum.2010.196 10.1186/s40659-015-0057-0 10.1186/s41232-019-0111-3 10.1038/nrd3930 10.1111/bph.14173 |
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| Keywords | Cartilage Signal transduction Inflammation mediators In vitro techniques Chondrocytes Phenols Extracellular matrix Oleocanthal Anti-inflammatory agents Osteoarthritis Protease-activated receptor 2 (PAR-2) Mitochondrial membrane potential |
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| References | NL Bergholt (7888_CR26) 2019; 10 LV Johnson (7888_CR20) 1981; 88 7888_CR7 M Scotece (7888_CR10) 2018; 49 7888_CR3 A Kahan (7888_CR59) 2009; 60 JK Fields (7888_CR67) 2019; 10 TL Chen (7888_CR71) 2011; 18 R Patnaik (7888_CR13) 2023; 12 DJ Wilkinson (7888_CR39) 2019; 176 7888_CR54 7888_CR52 7888_CR53 M Kapoor (7888_CR64) 2011; 7 X Ye (7888_CR78) 2021; 156 N Veronese (7888_CR6) 2019; 38 TJ Lu (7888_CR25) 2017; 26 S Kan (7888_CR86) 2021; 13 H Yoshitomi (7888_CR79) 2018; 9 T Ono (7888_CR90) 2020; 40 B Beutler (7888_CR15) 2000; 3 AN Ramey-Ward (7888_CR16) 2024; 32 S Jannati (7888_CR12) 2024; 25 A Latourte (7888_CR81) 2022; 30 C Boe (7888_CR55) 2015; 44 JT Liu (7888_CR87) 2010; 18 J Buckland (7888_CR48) 2013; 9 Y Henrotin (7888_CR57) 2012; 14 AE Koch (7888_CR70) 1992; 90 R Qu (7888_CR50) 2018; 32 S Kwak (7888_CR22) 2023; 12 GS Lazarus (7888_CR37) 1968; 47 WR Ferrell (7888_CR41) 2003; 111 R Ma (7888_CR89) 2012; 13 MW Carr (7888_CR68) 1994; 91 K McCulloch (7888_CR36) 2018; 9 YK Xu (7888_CR73) 2015; 48 K Jones (7888_CR77) 2022; 13 7888_CR32 R Patnaik (7888_CR11) 2023; 18 7888_CR33 YP Zhao (7888_CR47) 2015; 74 J Lozano-Castellon (7888_CR8) 2020; 60 7888_CR34 KJ Livak (7888_CR19) 2001; 25 E Fennema (7888_CR14) 2013; 31 7888_CR30 Y Zhao (7888_CR51) 2019; 41 7888_CR31 JM Milner (7888_CR38) 2010; 62 BA Michel (7888_CR58) 2005; 52 VI Grishko (7888_CR83) 2009; 17 P Mishra (7888_CR21) 2019; 22 FJ Blanco (7888_CR85) 2011; 7 Z Wu (7888_CR24) 2021; 4 H Tang (7888_CR75) 2022; 13 F Xu (7888_CR76) 2022; 152 HJ Hosea Blewett (7888_CR61) 2008; 48 SF Altschul (7888_CR18) 1990; 215 R Estruch (7888_CR1) 2018; 378 R Geng (7888_CR4) 2023; 26 N Veronese (7888_CR5) 2017; 36 Y Takahata (7888_CR27) 2019; 33 RC Billinghurst (7888_CR35) 1997; 99 M Croft (7888_CR46) 2013; 12 CR Scanzello (7888_CR65) 2017; 35 7888_CR29 L Jiang (7888_CR80) 2021; 8 7888_CR69 X Huang (7888_CR44) 2019; 11 P Zhu (7888_CR60) 2007; 122 F Ni (7888_CR72) 2020; 15 DB Zorov (7888_CR84) 2014; 94 CW Dieffenbach (7888_CR17) 1993; 3 7888_CR28 Y Xiang (7888_CR45) 2006; 14 7888_CR66 W Xiang (7888_CR82) 2023; 24 7888_CR23 MS Hayden (7888_CR49) 2014; 26 A Struglics (7888_CR74) 2006; 14 N Amiable (7888_CR88) 2009; 44 7888_CR62 L Lippiello (7888_CR56) 2008; 5 7888_CR63 S Kalogera (7888_CR43) 2021; 11 H Fan (7888_CR2) 2023; 15 GK Beauchamp (7888_CR9) 2005; 437 WR Ferrell (7888_CR40) 2010; 69 Q Lu (7888_CR42) 2017; 31 |
| References_xml | – volume: 122 start-page: 75 issue: 1 year: 2007 ident: 7888_CR60 publication-title: Clin Immunol doi: 10.1016/j.clim.2006.08.004 – volume: 8 start-page: 703110 year: 2021 ident: 7888_CR80 publication-title: Front Mol Biosci doi: 10.3389/fmolb.2021.703110 – volume: 18 start-page: e0290739 issue: 12 year: 2023 ident: 7888_CR11 publication-title: PLoS ONE doi: 10.1371/journal.pone.0290739 – volume: 69 start-page: 2051 issue: 11 year: 2010 ident: 7888_CR40 publication-title: Ann Rheum Dis doi: 10.1136/ard.2010.130336 – volume: 10 start-page: 1412 year: 2019 ident: 7888_CR67 publication-title: Front Immunol doi: 10.3389/fimmu.2019.01412 – ident: 7888_CR66 doi: 10.1084/jem.20191430 – volume: 26 start-page: 417 issue: 3 year: 2017 ident: 7888_CR25 publication-title: Cell Transpl doi: 10.3727/096368916X693464 – volume: 18 start-page: 43 issue: 1 year: 2011 ident: 7888_CR71 publication-title: J Biomed Sci doi: 10.1186/1423-0127-18-43 – volume: 47 start-page: 2622 issue: 12 year: 1968 ident: 7888_CR37 publication-title: J Clin Invest doi: 10.1172/JCI105945 – volume: 11 start-page: 24285 issue: 1 year: 2021 ident: 7888_CR43 publication-title: Sci Rep doi: 10.1038/s41598-021-03346-0 – volume: 44 start-page: 1143 issue: 6 year: 2009 ident: 7888_CR88 publication-title: Bone doi: 10.1016/j.bone.2009.02.015 – ident: 7888_CR33 – volume: 3 start-page: S30 issue: 3 year: 1993 ident: 7888_CR17 publication-title: PCR Methods Appl doi: 10.1101/gr.3.3.S30 – volume: 91 start-page: 3652 issue: 9 year: 1994 ident: 7888_CR68 publication-title: Proc Natl Acad Sci U S A doi: 10.1073/pnas.91.9.3652 – volume: 13 start-page: 789349 year: 2022 ident: 7888_CR77 publication-title: Front Immunol doi: 10.3389/fimmu.2022.789349 – ident: 7888_CR63 doi: 10.1155/2021/5558066 – volume: 60 start-page: 2532 issue: 15 year: 2020 ident: 7888_CR8 publication-title: Crit Rev Food Sci Nutr doi: 10.1080/10408398.2019.1650715 – volume: 24 start-page: 130 issue: 1 year: 2023 ident: 7888_CR82 publication-title: BMC Musculoskelet Disord doi: 10.1186/s12891-022-05949-8 – volume: 9 start-page: 257 year: 2018 ident: 7888_CR36 publication-title: Front Endocrinol (Lausanne) doi: 10.3389/fendo.2018.00257 – volume: 152 start-page: 155805 year: 2022 ident: 7888_CR76 publication-title: Cytokine doi: 10.1016/j.cyto.2022.155805 – volume: 14 start-page: 201 issue: 1 year: 2012 ident: 7888_CR57 publication-title: Arthritis Res Ther doi: 10.1186/ar3657 – ident: 7888_CR69 doi: 10.3390/ijms22179208 – volume: 14 start-page: 101 issue: 2 year: 2006 ident: 7888_CR74 publication-title: Osteoarthritis Cartilage doi: 10.1016/j.joca.2005.07.018 – volume: 38 start-page: 2735 issue: 6 year: 2019 ident: 7888_CR6 publication-title: Clin Nutr doi: 10.1016/j.clnu.2018.11.032 – volume: 18 start-page: 1218 issue: 9 year: 2010 ident: 7888_CR87 publication-title: Osteoarthritis Cartilage doi: 10.1016/j.joca.2010.07.003 – volume: 74 start-page: 2244 issue: 12 year: 2015 ident: 7888_CR47 publication-title: Ann Rheum Dis doi: 10.1136/annrheumdis-2014-205779 – volume: 60 start-page: 524 issue: 2 year: 2009 ident: 7888_CR59 publication-title: Arthritis Rheum doi: 10.1002/art.24255 – volume: 3 start-page: 23 issue: 1 year: 2000 ident: 7888_CR15 publication-title: Curr Opin Microbiol doi: 10.1016/S1369-5274(99)00046-6 – volume: 31 start-page: 108 issue: 2 year: 2013 ident: 7888_CR14 publication-title: Trends Biotechnol doi: 10.1016/j.tibtech.2012.12.003 – ident: 7888_CR28 doi: 10.1016/j.lfs.2012.09.012 – volume: 32 start-page: 257 issue: 3 year: 2024 ident: 7888_CR16 publication-title: Wound Repair Regen doi: 10.1111/wrr.13137 – volume: 11 start-page: 12532 issue: 24 year: 2019 ident: 7888_CR44 publication-title: Aging doi: 10.18632/aging.102586 – volume: 48 start-page: 458 issue: 5 year: 2008 ident: 7888_CR61 publication-title: Crit Rev Food Sci Nutr doi: 10.1080/10408390701429526 – volume: 13 start-page: 999851 year: 2022 ident: 7888_CR75 publication-title: Front Pharmacol doi: 10.3389/fphar.2022.999851 – volume: 30 start-page: 175 issue: 2 year: 2022 ident: 7888_CR81 publication-title: Osteoarthritis Cartilage doi: 10.1016/j.joca.2021.09.012 – volume: 90 start-page: 772 issue: 3 year: 1992 ident: 7888_CR70 publication-title: J Clin Invest doi: 10.1172/JCI115950 – ident: 7888_CR34 doi: 10.3390/nu9101060 – volume: 52 start-page: 779 issue: 3 year: 2005 ident: 7888_CR58 publication-title: Arthritis Rheum doi: 10.1002/art.20867 – volume: 26 start-page: 481 issue: 4 year: 2023 ident: 7888_CR4 publication-title: Exp Ther Med doi: 10.3892/etm.2023.12180 – volume: 17 start-page: 107 issue: 1 year: 2009 ident: 7888_CR83 publication-title: Osteoarthritis Cartilage doi: 10.1016/j.joca.2008.05.009 – ident: 7888_CR53 doi: 10.3390/ijms22147645 – ident: 7888_CR54 doi: 10.3390/biology12081061 – volume: 94 start-page: 909 issue: 3 year: 2014 ident: 7888_CR84 publication-title: Physiol Rev doi: 10.1152/physrev.00026.2013 – volume: 32 start-page: 1044 issue: 2 year: 2018 ident: 7888_CR50 publication-title: FASEB J doi: 10.1096/fj.201700265R – ident: 7888_CR3 doi: 10.3390/metabo10100392 – ident: 7888_CR7 doi: 10.3390/antiox12122112 – volume: 437 start-page: 45 issue: 7055 year: 2005 ident: 7888_CR9 publication-title: Nature doi: 10.1038/437045a – volume: 14 start-page: 1163 issue: 11 year: 2006 ident: 7888_CR45 publication-title: Osteoarthritis Cartilage doi: 10.1016/j.joca.2006.04.015 – volume: 33 start-page: 619 issue: 1 year: 2019 ident: 7888_CR27 publication-title: FASEB J doi: 10.1096/fj.201800259R – volume: 13 start-page: 154 year: 2012 ident: 7888_CR89 publication-title: BMC Musculoskelet Disord doi: 10.1186/1471-2474-13-154 – volume: 9 start-page: 3762 issue: 1 year: 2018 ident: 7888_CR79 publication-title: Nat Commun doi: 10.1038/s41467-018-06187-0 – volume: 13 start-page: S1102 issue: 2suppl year: 2021 ident: 7888_CR86 publication-title: Cartilage doi: 10.1177/19476035211063858 – volume: 215 start-page: 403 issue: 3 year: 1990 ident: 7888_CR18 publication-title: J Mol Biol doi: 10.1016/S0022-2836(05)80360-2 – volume: 62 start-page: 1955 issue: 7 year: 2010 ident: 7888_CR38 publication-title: Arthritis Rheum doi: 10.1002/art.27476 – volume: 22 start-page: 407 issue: 4 year: 2019 ident: 7888_CR21 publication-title: Ann Card Anaesth doi: 10.4103/aca.ACA_94_19 – volume: 41 start-page: 556 year: 2019 ident: 7888_CR51 publication-title: EBioMedicine doi: 10.1016/j.ebiom.2019.02.035 – volume: 7 start-page: 161 issue: 3 year: 2011 ident: 7888_CR85 publication-title: Nat Rev Rheumatol doi: 10.1038/nrrheum.2010.213 – volume: 25 start-page: 402 issue: 4 year: 2001 ident: 7888_CR19 publication-title: Methods doi: 10.1006/meth.2001.1262 – volume: 36 start-page: 1609 issue: 6 year: 2017 ident: 7888_CR5 publication-title: Clin Nutr doi: 10.1016/j.clnu.2016.09.035 – volume: 12 start-page: e42964 year: 2023 ident: 7888_CR13 publication-title: JMIR Res Protoc doi: 10.2196/42964 – volume: 44 start-page: 302 issue: 7 year: 2015 ident: 7888_CR55 publication-title: Am J Orthop (Belle Mead NJ) – volume: 5 start-page: 191 issue: 2 year: 2008 ident: 7888_CR56 publication-title: Evid Based Complement Alternat Med doi: 10.1093/ecam/nem132 – volume: 88 start-page: 526 issue: 3 year: 1981 ident: 7888_CR20 publication-title: J Cell Biol doi: 10.1083/jcb.88.3.526 – ident: 7888_CR31 doi: 10.3390/antiox10050650 – volume: 111 start-page: 35 issue: 1 year: 2003 ident: 7888_CR41 publication-title: J Clin Invest doi: 10.1172/JCI16913 – volume: 35 start-page: 735 issue: 4 year: 2017 ident: 7888_CR65 publication-title: J Orthop Res doi: 10.1002/jor.23471 – volume: 15 start-page: 107 issue: 1 year: 2023 ident: 7888_CR2 publication-title: Diabetol Metab Syndr doi: 10.1186/s13098-023-01052-7 – volume: 12 start-page: 89 issue: 2 year: 2023 ident: 7888_CR22 publication-title: J Lipid Atheroscler doi: 10.12997/jla.2023.12.2.89 – ident: 7888_CR30 doi: 10.1002/art.27437 – volume: 99 start-page: 1534 issue: 7 year: 1997 ident: 7888_CR35 publication-title: J Clin Invest doi: 10.1172/JCI119316 – volume: 26 start-page: 253 issue: 3 year: 2014 ident: 7888_CR49 publication-title: Semin Immunol doi: 10.1016/j.smim.2014.05.004 – ident: 7888_CR29 doi: 10.3390/ijerph13080755 – volume: 25 start-page: 8727 issue: 16 year: 2024 ident: 7888_CR12 publication-title: Int J Mol Sci doi: 10.3390/ijms25168727 – volume: 156 start-page: 111616 year: 2021 ident: 7888_CR78 publication-title: Exp Gerontol doi: 10.1016/j.exger.2021.111616 – volume: 378 start-page: e34 issue: 25 year: 2018 ident: 7888_CR1 publication-title: N Engl J Med doi: 10.1056/NEJMoa1800389 – volume: 15 start-page: 516 issue: 1 year: 2020 ident: 7888_CR72 publication-title: J Orthop Surg Res doi: 10.1186/s13018-020-02045-2 – ident: 7888_CR23 doi: 10.7554/eLife.36163 – volume: 9 start-page: 566 issue: 10 year: 2013 ident: 7888_CR48 publication-title: Nat Rev Rheumatol doi: 10.1038/nrrheum.2013.135 – ident: 7888_CR52 doi: 10.3390/ijms17122042 – ident: 7888_CR32 – volume: 31 start-page: 1517 issue: 12 year: 2017 ident: 7888_CR42 publication-title: Zhongguo Xiu Fu Chong Jian Wai Ke Za Zhi – volume: 4 start-page: 100030 year: 2021 ident: 7888_CR24 publication-title: Biomater Biosyst – volume: 10 start-page: 370 issue: 3 year: 2019 ident: 7888_CR26 publication-title: Cartilage doi: 10.1177/1947603518764262 – volume: 49 start-page: 2414 issue: 6 year: 2018 ident: 7888_CR10 publication-title: Cell Physiol Biochem doi: 10.1159/000493840 – ident: 7888_CR62 doi: 10.3390/medicina59020191 – volume: 7 start-page: 33 issue: 1 year: 2011 ident: 7888_CR64 publication-title: Nat Rev Rheumatol doi: 10.1038/nrrheum.2010.196 – volume: 48 start-page: 64 year: 2015 ident: 7888_CR73 publication-title: Biol Res doi: 10.1186/s40659-015-0057-0 – volume: 40 start-page: 2 year: 2020 ident: 7888_CR90 publication-title: Inflamm Regen doi: 10.1186/s41232-019-0111-3 – volume: 12 start-page: 147 issue: 2 year: 2013 ident: 7888_CR46 publication-title: Nat Rev Drug Discov doi: 10.1038/nrd3930 – volume: 176 start-page: 38 issue: 1 year: 2019 ident: 7888_CR39 publication-title: Br J Pharmacol doi: 10.1111/bph.14173 |
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| Snippet | Osteoarthritis (OA) is a prevalent degenerative joint disease characterized by chronic inflammation and progressive cartilage degradation, ultimately leading... Background Osteoarthritis (OA) is a prevalent degenerative joint disease characterized by chronic inflammation and progressive cartilage degradation,... BackgroundOsteoarthritis (OA) is a prevalent degenerative joint disease characterized by chronic inflammation and progressive cartilage degradation, ultimately... Abstract Background Osteoarthritis (OA) is a prevalent degenerative joint disease characterized by chronic inflammation and progressive cartilage degradation,... |
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| SubjectTerms | Aldehydes Analysis Anti-inflammatory agents Anti-Inflammatory Agents - pharmacology Antibiotics Apoptosis Bioenergetics Bone marrow Cartilage Cartilage cells Cartilage diseases Cell culture Cell differentiation Cell growth Cell receptors Cell viability Cells, Cultured Cellular signal transduction Chondrocytes Chondrocytes - drug effects Chondrocytes - metabolism Consent Cyclopentane Monoterpenes - pharmacology Diet therapy Down-regulation Enzymes Ethylenediaminetetraacetic acid Flow cytometry Fluorescent indicators Functional Food Functional foods Functional foods & nutraceuticals Gene expression Genes Health aspects Human subjects Humans In vitro techniques Inflammation Inflammation - drug therapy Inflammation - metabolism Joint diseases Lipopolysaccharides Lipopolysaccharides - pharmacology Membrane potential Membrane Potential, Mitochondrial - drug effects Mesenchymal stem cells Mesenchymal Stem Cells - drug effects Mesenchymal Stem Cells - metabolism Mitochondria Mitochondria - drug effects Mitochondria - metabolism Monocyte chemoattractant protein 1 Musculoskeletal diseases Nitrogen Nonsteroidal anti-inflammatory drugs Oleocanthal Olive oil Osteoarthritis Osteoarthritis - drug therapy Osteoarthritis - metabolism Pathogenesis Penicillin Phenolic compounds Phenols Polymerase chain reaction Protease-activated receptor 2 (PAR-2) Proteases Rankings Receptor, PAR-2 - metabolism Scientific equipment and supplies industry Stem cells Therapeutics, Experimental Tumor necrosis factor-TNF |
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| Title | Targeting PAR2-mediated inflammation in osteoarthritis: a comprehensive in vitro evaluation of oleocanthal’s potential as a functional food intervention for chondrocyte protection and anti-inflammatory effects |
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