α-Bisabolol Mitigates Colon Inflammation by Stimulating Colon PPAR-γ Transcription Factor: In Vivo and In Vitro Study
The incidence and prevalence of inflammatory bowel disease (IBD, Crohn’s disease, and ulcerative colitis) are increasing worldwide. The etiology of IBD is multifactorial, including genetic predisposition, dysregulated immune response, microbial dysbiosis, and environmental factors. However, many of...
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| Published in | PPAR research Vol. 2022; pp. 1 - 22 |
|---|---|
| Main Authors | , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Hindawi
2022
John Wiley & Sons, Inc Wiley |
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| Online Access | Get full text |
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| Abstract | The incidence and prevalence of inflammatory bowel disease (IBD, Crohn’s disease, and ulcerative colitis) are increasing worldwide. The etiology of IBD is multifactorial, including genetic predisposition, dysregulated immune response, microbial dysbiosis, and environmental factors. However, many of the existing therapies are associated with marked side effects. Therefore, the development of new drugs for IBD treatment is an important area of investigation. Here, we investigated the anti-inflammatory effects of α-bisabolol, a naturally occurring monocyclic sesquiterpene alcohol present in many aromatic plants, in colonic inflammation. To address this, we used molecular docking and dynamic studies to understand how α-bisabolol interacts with PPAR-γ, which is highly expressed in the colonic epithelium: in vivo (mice) and in vitro (RAW264.7 macrophages and HT-29 colonic adenocarcinoma cells) models. The molecular docking and dynamic analysis revealed that α-bisabolol interacts with PPAR-γ, a nuclear receptor protein that is highly expressed in the colon epithelium. Treatment with α-bisabolol in DSS-administered mice significantly reduced Disease Activity Index (DAI), myeloperoxidase (MPO) activity, and colonic length and protected the microarchitecture of the colon. α-Bisabolol treatment also reduced the expression of proinflammatory cytokines (IL-6, IL1β, TNF-α, and IL-17A) at the protein and mRNA levels. The expression of COX-2 and iNOS inflammatory mediators were reduced along with tissue nitrite levels. Furthermore, α-bisabolol decreased the phosphorylation of activated mitogen-activated protein kinase (MAPK) signaling and nuclear factor kappa B (NFκB) proteins and enhanced colon epithelial PPAR-γ transcription factor expression. However, the PPAR-α and β/δ expression was not altered, indicating α-bisabolol is a specific stimulator of PPAR-γ. α-Bisabolol also increased the PPAR-γ transcription factor expression but not PPAR-α and β/δ in pretreated in LPS-stimulated RAW264.7 macrophages. α-Bisabolol significantly decreased the expression of proinflammatory chemokines (CXCL-1 and IL-8) mRNA in HT-29 cells treated with TNF-α and HT-29 PPAR-γ promoter activity. These results demonstrate that α-bisabolol mitigates colonic inflammation by inhibiting MAPK signaling and stimulating PPAR-γ expression. |
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| AbstractList | The incidence and prevalence of inflammatory bowel disease (IBD, Crohn’s disease, and ulcerative colitis) are increasing worldwide. The etiology of IBD is multifactorial, including genetic predisposition, dysregulated immune response, microbial dysbiosis, and environmental factors. However, many of the existing therapies are associated with marked side effects. Therefore, the development of new drugs for IBD treatment is an important area of investigation. Here, we investigated the anti-inflammatory effects of α-bisabolol, a naturally occurring monocyclic sesquiterpene alcohol present in many aromatic plants, in colonic inflammation. To address this, we used molecular docking and dynamic studies to understand how α-bisabolol interacts with PPAR-γ, which is highly expressed in the colonic epithelium: in vivo (mice) and in vitro (RAW264.7 macrophages and HT-29 colonic adenocarcinoma cells) models. The molecular docking and dynamic analysis revealed that α-bisabolol interacts with PPAR-γ, a nuclear receptor protein that is highly expressed in the colon epithelium. Treatment with α-bisabolol in DSS-administered mice significantly reduced Disease Activity Index (DAI), myeloperoxidase (MPO) activity, and colonic length and protected the microarchitecture of the colon. α-Bisabolol treatment also reduced the expression of proinflammatory cytokines (IL-6, IL1β, TNF-α, and IL-17A) at the protein and mRNA levels. The expression of COX-2 and iNOS inflammatory mediators were reduced along with tissue nitrite levels. Furthermore, α-bisabolol decreased the phosphorylation of activated mitogen-activated protein kinase (MAPK) signaling and nuclear factor kappa B (NFκB) proteins and enhanced colon epithelial PPAR-γ transcription factor expression. However, the PPAR-α and β/δ expression was not altered, indicating α-bisabolol is a specific stimulator of PPAR-γ. α-Bisabolol also increased the PPAR-γ transcription factor expression but not PPAR-α and β/δ in pretreated in LPS-stimulated RAW264.7 macrophages. α-Bisabolol significantly decreased the expression of proinflammatory chemokines (CXCL-1 and IL-8) mRNA in HT-29 cells treated with TNF-α and HT-29 PPAR-γ promoter activity. These results demonstrate that α-bisabolol mitigates colonic inflammation by inhibiting MAPK signaling and stimulating PPAR-γ expression. The incidence and prevalence of inflammatory bowel disease (IBD, Crohn's disease, and ulcerative colitis) are increasing worldwide. The etiology of IBD is multifactorial, including genetic predisposition, dysregulated immune response, microbial dysbiosis, and environmental factors. However, many of the existing therapies are associated with marked side effects. Therefore, the development of new drugs for IBD treatment is an important area of investigation. Here, we investigated the anti-inflammatory effects of -bisabolol, a naturally occurring monocyclic sesquiterpene alcohol present in many aromatic plants, in colonic inflammation. To address this, we used molecular docking and dynamic studies to understand how -bisabolol interacts with PPAR- , which is highly expressed in the colonic epithelium: in vivo (mice) and in vitro (RAW264.7 macrophages and HT-29 colonic adenocarcinoma cells) models. The molecular docking and dynamic analysis revealed that -bisabolol interacts with PPAR- , a nuclear receptor protein that is highly expressed in the colon epithelium. Treatment with -bisabolol in DSS-administered mice significantly reduced Disease Activity Index (DAI), myeloperoxidase (MPO) activity, and colonic length and protected the microarchitecture of the colon. -Bisabolol treatment also reduced the expression of proinflammatory cytokines (IL-6, IL1 , TNF- , and IL-17A) at the protein and mRNA levels. The expression of COX-2 and iNOS inflammatory mediators were reduced along with tissue nitrite levels. Furthermore, -bisabolol decreased the phosphorylation of activated mitogen-activated protein kinase (MAPK) signaling and nuclear factor kappa B (NF B) proteins and enhanced colon epithelial PPAR- transcription factor expression. However, the PPAR- and / expression was not altered, indicating -bisabolol is a specific stimulator of PPAR- . -Bisabolol also increased the PPAR- transcription factor expression but not PPAR- and / in pretreated in LPS-stimulated RAW264.7 macrophages. -Bisabolol significantly decreased the expression of proinflammatory chemokines (CXCL-1 and IL-8) mRNA in HT-29 cells treated with TNF- and HT-29 PPAR- promoter activity. These results demonstrate that -bisabolol mitigates colonic inflammation by inhibiting MAPK signaling and stimulating PPAR- expression. The incidence and prevalence of inflammatory bowel disease (IBD, Crohn's disease, and ulcerative colitis) are increasing worldwide. The etiology of IBD is multifactorial, including genetic predisposition, dysregulated immune response, microbial dysbiosis, and environmental factors. However, many of the existing therapies are associated with marked side effects. Therefore, the development of new drugs for IBD treatment is an important area of investigation. Here, we investigated the anti-inflammatory effects of α-bisabolol, a naturally occurring monocyclic sesquiterpene alcohol present in many aromatic plants, in colonic inflammation. To address this, we used molecular docking and dynamic studies to understand how α-bisabolol interacts with PPAR-γ, which is highly expressed in the colonic epithelium: in vivo (mice) and in vitro (RAW264.7 macrophages and HT-29 colonic adenocarcinoma cells) models. The molecular docking and dynamic analysis revealed that α-bisabolol interacts with PPAR-γ, a nuclear receptor protein that is highly expressed in the colon epithelium. Treatment with α-bisabolol in DSS-administered mice significantly reduced Disease Activity Index (DAI), myeloperoxidase (MPO) activity, and colonic length and protected the microarchitecture of the colon. α-Bisabolol treatment also reduced the expression of proinflammatory cytokines (IL-6, IL1β, TNF-α, and IL-17A) at the protein and mRNA levels. The expression of COX-2 and iNOS inflammatory mediators were reduced along with tissue nitrite levels. Furthermore, α-bisabolol decreased the phosphorylation of activated mitogen-activated protein kinase (MAPK) signaling and nuclear factor kappa B (NFκB) proteins and enhanced colon epithelial PPAR-γ transcription factor expression. However, the PPAR-α and β/δ expression was not altered, indicating α-bisabolol is a specific stimulator of PPAR-γ. α-Bisabolol also increased the PPAR-γ transcription factor expression but not PPAR-α and β/δ in pretreated in LPS-stimulated RAW264.7 macrophages. α-Bisabolol significantly decreased the expression of proinflammatory chemokines (CXCL-1 and IL-8) mRNA in HT-29 cells treated with TNF-α and HT-29 PPAR-γ promoter activity. These results demonstrate that α-bisabolol mitigates colonic inflammation by inhibiting MAPK signaling and stimulating PPAR-γ expression.The incidence and prevalence of inflammatory bowel disease (IBD, Crohn's disease, and ulcerative colitis) are increasing worldwide. The etiology of IBD is multifactorial, including genetic predisposition, dysregulated immune response, microbial dysbiosis, and environmental factors. However, many of the existing therapies are associated with marked side effects. Therefore, the development of new drugs for IBD treatment is an important area of investigation. Here, we investigated the anti-inflammatory effects of α-bisabolol, a naturally occurring monocyclic sesquiterpene alcohol present in many aromatic plants, in colonic inflammation. To address this, we used molecular docking and dynamic studies to understand how α-bisabolol interacts with PPAR-γ, which is highly expressed in the colonic epithelium: in vivo (mice) and in vitro (RAW264.7 macrophages and HT-29 colonic adenocarcinoma cells) models. The molecular docking and dynamic analysis revealed that α-bisabolol interacts with PPAR-γ, a nuclear receptor protein that is highly expressed in the colon epithelium. Treatment with α-bisabolol in DSS-administered mice significantly reduced Disease Activity Index (DAI), myeloperoxidase (MPO) activity, and colonic length and protected the microarchitecture of the colon. α-Bisabolol treatment also reduced the expression of proinflammatory cytokines (IL-6, IL1β, TNF-α, and IL-17A) at the protein and mRNA levels. The expression of COX-2 and iNOS inflammatory mediators were reduced along with tissue nitrite levels. Furthermore, α-bisabolol decreased the phosphorylation of activated mitogen-activated protein kinase (MAPK) signaling and nuclear factor kappa B (NFκB) proteins and enhanced colon epithelial PPAR-γ transcription factor expression. However, the PPAR-α and β/δ expression was not altered, indicating α-bisabolol is a specific stimulator of PPAR-γ. α-Bisabolol also increased the PPAR-γ transcription factor expression but not PPAR-α and β/δ in pretreated in LPS-stimulated RAW264.7 macrophages. α-Bisabolol significantly decreased the expression of proinflammatory chemokines (CXCL-1 and IL-8) mRNA in HT-29 cells treated with TNF-α and HT-29 PPAR-γ promoter activity. These results demonstrate that α-bisabolol mitigates colonic inflammation by inhibiting MAPK signaling and stimulating PPAR-γ expression. The incidence and prevalence of inflammatory bowel disease (IBD, Crohn's disease, and ulcerative colitis) are increasing worldwide. The etiology of IBD is multifactorial, including genetic predisposition, dysregulated immune response, microbial dysbiosis, and environmental factors. However, many of the existing therapies are associated with marked side effects. Therefore, the development of new drugs for IBD treatment is an important area of investigation. Here, we investigated the anti-inflammatory effects of α -bisabolol, a naturally occurring monocyclic sesquiterpene alcohol present in many aromatic plants, in colonic inflammation. To address this, we used molecular docking and dynamic studies to understand how α -bisabolol interacts with PPAR-γ , which is highly expressed in the colonic epithelium: in vivo (mice) and in vitro (RAW264.7 macrophages and HT-29 colonic adenocarcinoma cells) models. The molecular docking and dynamic analysis revealed that α -bisabolol interacts with PPAR-γ , a nuclear receptor protein that is highly expressed in the colon epithelium. Treatment with α -bisabolol in DSS-administered mice significantly reduced Disease Activity Index (DAI), myeloperoxidase (MPO) activity, and colonic length and protected the microarchitecture of the colon. α -Bisabolol treatment also reduced the expression of proinflammatory cytokines (IL-6, IL1β , TNF-α , and IL-17A) at the protein and mRNA levels. The expression of COX-2 and iNOS inflammatory mediators were reduced along with tissue nitrite levels. Furthermore, α -bisabolol decreased the phosphorylation of activated mitogen-activated protein kinase (MAPK) signaling and nuclear factor kappa B (NFκ B) proteins and enhanced colon epithelial PPAR-γ transcription factor expression. However, the PPAR-α and β /δ expression was not altered, indicating α -bisabolol is a specific stimulator of PPAR-γ . α -Bisabolol also increased the PPAR-γ transcription factor expression but not PPAR-α and β /δ in pretreated in LPS-stimulated RAW264.7 macrophages. α -Bisabolol significantly decreased the expression of proinflammatory chemokines (CXCL-1 and IL-8) mRNA in HT-29 cells treated with TNF-α and HT-29 PPAR-γ promoter activity. These results demonstrate that α -bisabolol mitigates colonic inflammation by inhibiting MAPK signaling and stimulating PPAR-γ expression. The incidence and prevalence of inflammatory bowel disease (IBD, Crohn's disease, and ulcerative colitis) are increasing worldwide. The etiology of IBD is multifactorial, including genetic predisposition, dysregulated immune response, microbial dysbiosis, and environmental factors. However, many of the existing therapies are associated with marked side effects. Therefore, the development of new drugs for IBD treatment is an important area of investigation. Here, we investigated the anti-inflammatory effects of α -bisabolol, a naturally occurring monocyclic sesquiterpene alcohol present in many aromatic plants, in colonic inflammation. To address this, we used molecular docking and dynamic studies to understand how α -bisabolol interacts with PPAR- γ , which is highly expressed in the colonic epithelium: in vivo (mice) and in vitro (RAW264.7 macrophages and HT-29 colonic adenocarcinoma cells) models. The molecular docking and dynamic analysis revealed that α -bisabolol interacts with PPAR- γ , a nuclear receptor protein that is highly expressed in the colon epithelium. Treatment with α -bisabolol in DSS-administered mice significantly reduced Disease Activity Index (DAI), myeloperoxidase (MPO) activity, and colonic length and protected the microarchitecture of the colon. α -Bisabolol treatment also reduced the expression of proinflammatory cytokines (IL-6, IL1 β , TNF- α , and IL-17A) at the protein and mRNA levels. The expression of COX-2 and iNOS inflammatory mediators were reduced along with tissue nitrite levels. Furthermore, α -bisabolol decreased the phosphorylation of activated mitogen-activated protein kinase (MAPK) signaling and nuclear factor kappa B (NF κ B) proteins and enhanced colon epithelial PPAR- γ transcription factor expression. However, the PPAR- α and β / δ expression was not altered, indicating α -bisabolol is a specific stimulator of PPAR- γ . α -Bisabolol also increased the PPAR- γ transcription factor expression but not PPAR- α and β / δ in pretreated in LPS-stimulated RAW264.7 macrophages. α -Bisabolol significantly decreased the expression of proinflammatory chemokines (CXCL-1 and IL-8) mRNA in HT-29 cells treated with TNF- α and HT-29 PPAR- γ promoter activity. These results demonstrate that α -bisabolol mitigates colonic inflammation by inhibiting MAPK signaling and stimulating PPAR- γ expression. |
| Audience | Academic |
| Author | Dudeja, Pradeep K. Adrian, Thomas E. Almarzooqi, Saeeda Subramanya, Sandeep B. Patil, Rajesh B. Venkataraman, Balaji Ojha, Shreesh K. Raj, Vishnu Attoub, Samir Bhongade, Bhoomendra A. |
| AuthorAffiliation | 9 Department of Basic Medical Sciences, College of Medicine, Mohammed Bin Rashid University of Medicine and Health Sciences, PO Box—505055, Dubai, UAE 3 Department of Pathology, College of Medicine and Health Sciences, United Arab Emirates University, PO Box—17666, Al Ain, UAE 4 Jesse Brown Veterans Affairs Medical Center, Chicago, Illinois, USA 6 Department of Pharmaceutical Chemistry, RAK College of Pharmaceutical Chemistry, RAK Medical & Health Sciences University, Ras Al Khaimah, UAE 7 Department of Pharmaceutical Chemistry, STES's Smt. Kashibai Navale College of Pharmacy, Kondhwa (Bk), Pune, India 1 Department of Physiology, College of Medicine and Health Sciences, United Arab Emirates University, PO Box—17666, Al Ain, UAE 5 Division of Gastroenterology and Hepatology, Department of Medicine, University of Illinois at Chicago, Chicago, Illinois, USA 8 Department of Pharmacology and Therapeutics, College of Medicine and Health Sciences, United Arab Emirates University, PO Box—17666, Al Ai |
| AuthorAffiliation_xml | – name: 4 Jesse Brown Veterans Affairs Medical Center, Chicago, Illinois, USA – name: 3 Department of Pathology, College of Medicine and Health Sciences, United Arab Emirates University, PO Box—17666, Al Ain, UAE – name: 6 Department of Pharmaceutical Chemistry, RAK College of Pharmaceutical Chemistry, RAK Medical & Health Sciences University, Ras Al Khaimah, UAE – name: 8 Department of Pharmacology and Therapeutics, College of Medicine and Health Sciences, United Arab Emirates University, PO Box—17666, Al Ain, UAE – name: 9 Department of Basic Medical Sciences, College of Medicine, Mohammed Bin Rashid University of Medicine and Health Sciences, PO Box—505055, Dubai, UAE – name: 1 Department of Physiology, College of Medicine and Health Sciences, United Arab Emirates University, PO Box—17666, Al Ain, UAE – name: 5 Division of Gastroenterology and Hepatology, Department of Medicine, University of Illinois at Chicago, Chicago, Illinois, USA – name: 7 Department of Pharmaceutical Chemistry, STES's Smt. Kashibai Navale College of Pharmacy, Kondhwa (Bk), Pune, India – name: 2 Zayed Bin Sultan Center for Health Sciences, College of Medicine and Health Sciences, United Arab Emirates University, PO Box—17666, Al Ain, UAE |
| Author_xml | – sequence: 1 givenname: Balaji orcidid: 0000-0001-6561-2399 surname: Venkataraman fullname: Venkataraman, Balaji organization: Department of PhysiologyCollege of Medicine and Health SciencesUnited Arab Emirates UniversityPO Box—17666Al AinUAEuaeu.ac.ae – sequence: 2 givenname: Saeeda orcidid: 0000-0002-5147-0657 surname: Almarzooqi fullname: Almarzooqi, Saeeda organization: Department of PathologyCollege of Medicine and Health SciencesUnited Arab Emirates UniversityPO Box—17666Al AinUAEuaeu.ac.ae – sequence: 3 givenname: Vishnu orcidid: 0000-0002-2478-2225 surname: Raj fullname: Raj, Vishnu organization: Department of PhysiologyCollege of Medicine and Health SciencesUnited Arab Emirates UniversityPO Box—17666Al AinUAEuaeu.ac.ae – sequence: 4 givenname: Pradeep K. orcidid: 0000-0003-2252-7703 surname: Dudeja fullname: Dudeja, Pradeep K. organization: Jesse Brown Veterans Affairs Medical CenterChicagoIllinoisUSAchicago-health-care – sequence: 5 givenname: Bhoomendra A. orcidid: 0000-0002-4057-7125 surname: Bhongade fullname: Bhongade, Bhoomendra A. organization: Department of Pharmaceutical ChemistryRAK College of Pharmaceutical ChemistryRAK Medical & Health Sciences UniversityRas Al KhaimahUAErakmhsu.com – sequence: 6 givenname: Rajesh B. orcidid: 0000-0003-2986-9546 surname: Patil fullname: Patil, Rajesh B. organization: Department of Pharmaceutical ChemistrySTES’s Smt. Kashibai Navale College of PharmacyKondhwa (Bk)PuneIndia – sequence: 7 givenname: Shreesh K. orcidid: 0000-0001-7801-2966 surname: Ojha fullname: Ojha, Shreesh K. organization: Department of Pharmacology and TherapeuticsCollege of Medicine and Health SciencesUnited Arab Emirates UniversityPO Box—17666Al AinUAEuaeu.ac.ae – sequence: 8 givenname: Samir orcidid: 0000-0001-5862-9512 surname: Attoub fullname: Attoub, Samir organization: Department of Pharmacology and TherapeuticsCollege of Medicine and Health SciencesUnited Arab Emirates UniversityPO Box—17666Al AinUAEuaeu.ac.ae – sequence: 9 givenname: Thomas E. orcidid: 0000-0002-5051-1111 surname: Adrian fullname: Adrian, Thomas E. organization: Department of Basic Medical SciencesCollege of MedicineMohammed Bin Rashid University of Medicine and Health SciencesPO Box—505055DubaiUAEmbruniversity.ac.ae – sequence: 10 givenname: Sandeep B. orcidid: 0000-0002-4802-500X surname: Subramanya fullname: Subramanya, Sandeep B. organization: Department of PhysiologyCollege of Medicine and Health SciencesUnited Arab Emirates UniversityPO Box—17666Al AinUAEuaeu.ac.ae |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/35465355$$D View this record in MEDLINE/PubMed |
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| ContentType | Journal Article |
| Copyright | Copyright © 2022 Balaji Venkataraman et al. COPYRIGHT 2022 John Wiley & Sons, Inc. Copyright © 2022 Balaji Venkataraman et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. https://creativecommons.org/licenses/by/4.0 Copyright © 2022 Balaji Venkataraman et al. 2022 |
| Copyright_xml | – notice: Copyright © 2022 Balaji Venkataraman et al. – notice: COPYRIGHT 2022 John Wiley & Sons, Inc. – notice: Copyright © 2022 Balaji Venkataraman et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. https://creativecommons.org/licenses/by/4.0 – notice: Copyright © 2022 Balaji Venkataraman et al. 2022 |
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| SubjectTerms | Adenocarcinoma Animals Binding sites Cancer Cell culture Chemokines Colon Colon cancer Crohn's disease Cyclooxygenase-2 Cytokines Development and progression Drug development Dysbacteriosis Environmental factors Epithelium Etiology Gene expression Hydrogen bonds Immune response Immunosuppressive agents Inflammation Inflammatory bowel disease Inflammatory bowel diseases Interleukin 1 Interleukin 6 Interleukin 8 Ligands Lipopolysaccharides Macrophages MAP kinase Molecular modelling NF-κB protein Peroxidase Protein kinase Protein kinases Proteins Simulation Ulcerative colitis |
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| Title | α-Bisabolol Mitigates Colon Inflammation by Stimulating Colon PPAR-γ Transcription Factor: In Vivo and In Vitro Study |
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