Ferulic acid exerts neuroprotective effects against cerebral ischemia/reperfusion-induced injury via antioxidant and anti-apoptotic mechanisms in vitro and in vivo

Ferulic acid (FA) is a derivative of cinnamic acid. It is used in the treatment of heart head blood-vessel disease and exerts protective effects against hypoxia/ischemia-induced cell injury in the brain. This study investigated the potential neuroprotective effects of FA against ischemia/reperfusion...

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Published in	International journal of molecular medicine Vol. 40; no. 5; pp. 1444 - 1456
Main Authors	Ren, Zhongkun, Zhang, Rongping, Li, Yuanyuan, Li, Yu, Yang, Zhiyong, Yang, Hui
Format	Journal Article
Language	English
Published	Greece D.A. Spandidos 01.11.2017 Spandidos Publications Spandidos Publications UK Ltd
Subjects	Adapter proteins Animals Antioxidants Antioxidants - chemistry Antioxidants - pharmacology Apoptosis Apoptosis - drug effects Brain injuries Cardiovascular disease Care and treatment Cell Line Cells, Cultured Coumaric Acids - chemistry Coumaric Acids - pharmacology Disease Models, Animal Drug dosages ferulic acid Free radicals Gamma oryzanol Glutathione Peroxidase - metabolism Health aspects Hippocampus - metabolism Hippocampus - pathology Hypoglycemia Hypoxia Ischemia ischemia/reperfusion Male Malondialdehyde - metabolism Memory - drug effects Myeloid Differentiation Factor 88 - metabolism Nervous system Neuroprotective Agents - chemistry Neuroprotective Agents - pharmacology neuroprotective effect oxidation Oxidative stress Oxidative Stress - drug effects Pyramidal Cells - drug effects Pyramidal Cells - metabolism Rats Reactive oxygen species Reactive Oxygen Species - metabolism Reperfusion injury Reperfusion Injury - drug therapy Reperfusion Injury - metabolism Reperfusion Injury - pathology Rodents Signal Transduction - drug effects Studies Substance abuse treatment Toll-Like Receptors - metabolism Traditional Chinese medicine
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Abstract	Ferulic acid (FA) is a derivative of cinnamic acid. It is used in the treatment of heart head blood-vessel disease and exerts protective effects against hypoxia/ischemia-induced cell injury in the brain. This study investigated the potential neuroprotective effects of FA against ischemia/reperfusion (I/R)-induced brain injury in vivo and in vitro through hematoxylin and eosin (H&E) and Nissl staining assays, flow cytometry, Hoechst 33258 staining, quantitative PCR, western blot analysis and fluorescence microscopic analysis. In this study, models of cerebral I/R injury were established using rats and pheochromocytoma (PC-12) cells. The results revealed that treatment with FA significantly attenuated memory impairment, and reduced hippocampal neuronal apoptosis and oxidative stress in a dose-dependent manner. The results from in vitro experiments also indicated that FA protected the PC-12 cells against I/R-induced reactive oxygen species (ROS) generation and apoptosis by inhibiting apoptosis, Ca2+ influx, superoxide anion (O2−), malondialdehyde (MDA) and glutathione peroxidase (GSH-Px) production in a concentration-dependent manner. Moreover, FA inactivated the Toll-like receptor (TLR)/myeloid differentiation factor 88 (MyD88) pathway. MyD88 overexpression abolished the neuroprotective effects of FA. On the whole, we found that FA attenuated memory dysfunction and exerted protective effects against oxidative stress and apoptosis induced by I/R injury by inhibiting the TLR4/MyD88 signaling pathway. This study supports the view that FA may be a promising neuroprotective agent for use in the treatment of cerebral ischemia.
AbstractList	Ferulic acid (FA) is a derivative of cinnamic acid. It is used in the treatment of heart head blood-vessel disease and exerts protective effects against hypoxia/ischemia-induced cell injury in the brain. This study investigated the potential neuroprotective effects of FA against ischemia/reperfusion (I/R)-induced brain injury in vivo and in vitro through hematoxylin and eosin (H&E) and Nissl staining assays, flow cytometry, Hoechst 33258 staining, quantitative PCR, western blot analysis and fluorescence microscopic analysis. In this study, models of cerebral I/R injury were established using rats and pheochromocytoma (PC-12) cells. The results revealed that treatment with FA significantly attenuated memory impairment, and reduced hippocampal neuronal apoptosis and oxidative stress in a dose-dependent manner. The results from in vitro experiments also indicated that FA protected the PC-12 cells against I/R-induced reactive oxygen species (ROS) generation and apoptosis by inhibiting apoptosis, Ca2+ influx, superoxide anion (O2-), malondialdehyde (MDA) and glutathione peroxidase (GSH-Px) production in a concentration-dependent manner. Moreover, FA inactivated the Toll-like receptor (TLR)/myeloid differentiation factor 88 (MyD88) pathway. MyD88 overexpression abolished the neuroprotective effects of FA. On the whole, we found that FA attenuated memory dysfunction and exerted protective effects against oxidative stress and apoptosis induced by I/R injury by inhibiting the TLR4/MyD88 signaling pathway. This study supports the view that FA may be a promising neuroprotective agent for use in the treatment of cerebral ischemia. Ferulic acid (FA) is a derivative of cinnamic acid. It is used in the treatment of heart head blood-vessel disease and exerts protective effects against hypoxia/ischemia-induced cell injury in the brain. This study investigated the potential neuroprotective effects of FA against ischemia/reperfusion (I/R)-induced brain injury in vivo and in vitro through hematoxylin and eosin (H&E) and Nissl staining assays, flow cytometry, Hoechst 33258 staining, quantitative PCR, western blot analysis and fluorescence microscopic analysis. In this study, models of cerebral I/R injury were established using rats and pheochromocytoma (PC-12) cells. The results revealed that treatment with FA significantly attenuated memory impairment, and reduced hippocampal neuronal apoptosis and oxidative stress in a dose-dependent manner. The results from in vitro experiments also indicated that FA protected the PC-12 cells against I/R-induced reactive oxygen species (ROS) generation and apoptosis by inhibiting apoptosis, Ca 2+ influx, superoxide anion (O 2 − ), malondialdehyde (MDA) and glutathione peroxidase (GSH-Px) production in a concentration-dependent manner. Moreover, FA inactivated the Toll-like receptor (TLR)/myeloid differentiation factor 88 (MyD88) pathway. MyD88 overexpression abolished the neuroprotective effects of FA. On the whole, we found that FA attenuated memory dysfunction and exerted protective effects against oxidative stress and apoptosis induced by I/R injury by inhibiting the TLR4/MyD88 signaling pathway. This study supports the view that FA may be a promising neuroprotective agent for use in the treatment of cerebral ischemia. Ferulic acid (FA) is a derivative of cinnamic acid. It is used in the treatment of heart head blood-vessel disease and exerts protective effects against hypoxia/ischemia-induced cell injury in the brain. This study investigated the potential neuroprotective effects of FA against ischemia/reperfusion (I/R)-induced brain injury in vivo and in vitro through hematoxylin and eosin (H&E) and Nissl staining assays, flow cytometry, Hoechst 33258 staining, quantitative PCR, western blot analysis and fluorescence microscopic analysis. In this study, models of cerebral I/R injury were established using rats and pheochromocytoma (PC-12) cells. The results revealed that treatment with FA significantly attenuated memory impairment, and reduced hippocampal neuronal apoptosis and oxidative stress in a dose-dependent manner. The results from in vitro experiments also indicated that FA protected the PC-12 cells against I/R-induced reactive oxygen species (ROS) generation and apoptosis by inhibiting apoptosis, Ca2+ influx, superoxide anion (O2−), malondialdehyde (MDA) and glutathione peroxidase (GSH-Px) production in a concentration-dependent manner. Moreover, FA inactivated the Toll-like receptor (TLR)/myeloid differentiation factor 88 (MyD88) pathway. MyD88 overexpression abolished the neuroprotective effects of FA. On the whole, we found that FA attenuated memory dysfunction and exerted protective effects against oxidative stress and apoptosis induced by I/R injury by inhibiting the TLR4/MyD88 signaling pathway. This study supports the view that FA may be a promising neuroprotective agent for use in the treatment of cerebral ischemia. Ferulic acid (FA) is a derivative of cinnamic acid. It is used in the treatment of heart head blood-vessel disease and exerts protective effects against hypoxia/ischemia-induced cell injury in the brain. This study investigated the potential neuroprotective effects of FA against ischemia/reperfusion (I/R)-induced brain injury in vivo and in vitro through hematoxylin and eosin (H&E) and Nissl staining assays, flow cytometry, Hoechst 33258 staining, quantitative PCR, western blot analysis and fluorescence microscopic analysis. In this study, models of cerebral I/R injury were established using rats and pheochromocytoma (PC-12) cells. The results revealed that treatment with FA significantly attenuated memory impairment, and reduced hippocampal neuronal apoptosis and oxidative stress in a dose-dependent manner. The results from in vitro experiments also indicated that FA protected the PC-12 cells against I/R-induced reactive oxygen species (ROS) generation and apoptosis by inhibiting apoptosis, [Ca.sup.2+] influx, superoxide anion ([O.sub.2.sup.-]), malondialdehyde (MDA) and glutathione peroxidase (GSH-Px) production in a concentration-dependent manner. Moreover, FA inactivated the Toll-like receptor (TLR)/myeloid differentiation factor 88 (MyD88) pathway. MyD88 overexpression abolished the neuroprotective effects of FA. On the whole, we found that FA attenuated memory dysfunction and exerted protective effects against oxidative stress and apoptosis induced by I/R injury by inhibiting the TLR4/MyD88 signaling pathway. This study supports the view that FA may be a promising neuroprotective agent for use in the treatment of cerebral ischemia.
Audience	Academic
Author	Li, Yu Zhang, Rongping Ren, Zhongkun Li, Yuanyuan Yang, Zhiyong Yang, Hui
AuthorAffiliation	2 Biomedical Engineering Center, Kunming Medical University, Kunming, Yunnan 650500, P.R. China 1 Department of Neurosurgery, The First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan 650032
AuthorAffiliation_xml	– name: 2 Biomedical Engineering Center, Kunming Medical University, Kunming, Yunnan 650500, P.R. China – name: 1 Department of Neurosurgery, The First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan 650032
Author_xml	– sequence: 1 givenname: Zhongkun surname: Ren fullname: Ren, Zhongkun organization: Department of Neurosurgery, The First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan 650032 – sequence: 2 givenname: Rongping surname: Zhang fullname: Zhang, Rongping organization: Biomedical Engineering Center, Kunming Medical University, Kunming, Yunnan 650500, P.R. China – sequence: 3 givenname: Yuanyuan surname: Li fullname: Li, Yuanyuan organization: Department of Neurosurgery, The First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan 650032 – sequence: 4 givenname: Yu surname: Li fullname: Li, Yu organization: Department of Neurosurgery, The First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan 650032 – sequence: 5 givenname: Zhiyong surname: Yang fullname: Yang, Zhiyong organization: Department of Neurosurgery, The First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan 650032 – sequence: 6 givenname: Hui surname: Yang fullname: Yang, Hui organization: Biomedical Engineering Center, Kunming Medical University, Kunming, Yunnan 650500, P.R. China
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/28901374$$D View this record in MEDLINE/PubMed
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Copyright	Copyright: © Ren et al. COPYRIGHT 2017 Spandidos Publications Copyright Spandidos Publications UK Ltd. 2017 Copyright: © Ren et al. 2017
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PublicationCentury	2000
PublicationDate	2017-11-01
PublicationDateYYYYMMDD	2017-11-01
PublicationDate_xml	– month: 11 year: 2017 text: 2017-11-01 day: 01
PublicationDecade	2010
PublicationPlace	Greece
PublicationPlace_xml	– name: Greece – name: Athens
PublicationTitle	International journal of molecular medicine
PublicationTitleAlternate	Int J Mol Med
PublicationYear	2017
Publisher	D.A. Spandidos Spandidos Publications Spandidos Publications UK Ltd
Publisher_xml	– name: D.A. Spandidos – name: Spandidos Publications – name: Spandidos Publications UK Ltd
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Snippet	Ferulic acid (FA) is a derivative of cinnamic acid. It is used in the treatment of heart head blood-vessel disease and exerts protective effects against...
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SubjectTerms	Adapter proteins Animals Antioxidants Antioxidants - chemistry Antioxidants - pharmacology Apoptosis Apoptosis - drug effects Brain injuries Cardiovascular disease Care and treatment Cell Line Cells, Cultured Coumaric Acids - chemistry Coumaric Acids - pharmacology Disease Models, Animal Drug dosages ferulic acid Free radicals Gamma oryzanol Glutathione Peroxidase - metabolism Health aspects Hippocampus - metabolism Hippocampus - pathology Hypoglycemia Hypoxia Ischemia ischemia/reperfusion Male Malondialdehyde - metabolism Memory - drug effects Myeloid Differentiation Factor 88 - metabolism Nervous system Neuroprotective Agents - chemistry Neuroprotective Agents - pharmacology neuroprotective effect oxidation Oxidative stress Oxidative Stress - drug effects Pyramidal Cells - drug effects Pyramidal Cells - metabolism Rats Reactive oxygen species Reactive Oxygen Species - metabolism Reperfusion injury Reperfusion Injury - drug therapy Reperfusion Injury - metabolism Reperfusion Injury - pathology Rodents Signal Transduction - drug effects Studies Substance abuse treatment Toll-Like Receptors - metabolism Traditional Chinese medicine
Title	Ferulic acid exerts neuroprotective effects against cerebral ischemia/reperfusion-induced injury via antioxidant and anti-apoptotic mechanisms in vitro and in vivo
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