Premium
[6]‐Gingerol Ameliorates ISO‐Induced Myocardial Fibrosis by Reducing Oxidative Stress, Inflammation, and Apoptosis through Inhibition of TLR4/MAPKs/NF‐κB Pathway
Author(s) -
Han Xue,
Liu Panpan,
Liu Miaomiao,
Wei Ziheng,
Fan Sen,
Wang Xiangting,
Sun Shijiang,
Chu Li
Publication year - 2020
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.202000003
Subject(s) - oxidative stress , pharmacology , inflammation , chemistry , glutathione , fibrosis , p38 mitogen activated protein kinases , reactive oxygen species , superoxide dismutase , kinase , apoptosis , myocardial fibrosis , malondialdehyde , medicine , biochemistry , protein kinase a , enzyme
Scope [6]‐Gingerol is one of the primary pungent constituents of ginger. While [6]‐gingerol has many pharmacological effects, its benefits for myocardial fibrosis, including its exact role and underlying mechanisms, remain largely unexplored. The present study is designed to characterize the cardio‐protective effects of [6]‐gingerol in myocardial fibrosis mice and possible underlying mechanisms. Methods and results Mice are subcutaneously injected with isoproterenol (ISO, 10 mg kg −1 ) and gavaged with [6]‐gingerol (10, 20 mg kg −1 day −1 ) for 14 days. Pathological alterations, fibrosis, oxidative stress, inflammation response, and apoptosis are examined. In ISO‐induced myocardial fibrosis, [6]‐gingerol treatment decreases the J‐point, heart rate, cardiac weight index, left ventricle weight index, creatine kinase (CK), and lactate dehydrogenase serum levels, calcium concentration, reactive oxygen species, malondialdehyde, and glutathione disulfide (GSSG), and increases levels of superoxide dismutase, catalase, glutathione, and GSH/GSSG. Further, [6]‐gingerol improved ISO‐induced morphological pathologies, inhibited inflammation and apoptosis, and suppressed the toll‐like receptor‐4 (TLR4)/mitogen‐activated protein kinases (MAPKs)/nuclear factor κB (NF‐κB) signaling pathways. Conclusion The protective effect of [6]‐gingerol in mice with ISO‐induced myocardial fibrosis may be related to the inhibition of oxidative stress, inflammation, and apoptosis, potentially through the TLR4/MAPKs/NF‐κB signaling pathway.