Cardioprotection of vitexin on myocardial ischemia/reperfusion injury in rat via regulating inflammatory cytokines and MAPK pathway.
This study was conducted to demonstrate myocardial protective effects and possible underlying mechanisms of vitexin on myocardial ischemia/reperfusion (I/R) injury in rats. Occluding the anterior descending artery for 30 min and restoring blood perfusion for 60 min in rat established a model of myocardial I/R. The elevation of the ST segment of Electrocardiograph (ECG) was observed. The infarct size of the rat heart was assessed by triphenyltetrazolium chloride staining (TTC). LDH, CK, SOD activities and MDA content were determined. An immunohistochemical analysis was applied to measure the expression of myocardial NF-κBp65 and TNF-α. ERK/phospho-ERKand c-Jun/phospho-c-Jun protein expression was examined via Western Blot. Vitexin significantly reduced the elevation of the ST segment of ECG and myocardial infarct size. LDH and CK activities and MDA content were attenuated in serum, while SOD activity was markedly enhanced. Vitexin significantly attenuated I/R-induced increases of myocardial NF-κB and TNF-α. Moreover, Western Blot analysis presented that vitexin markedly enhanced the expression of phospho-ERK and weakened the expression of phospho-c-Jun compared to I/R group. The significant protective effect against myocardial ischemical/reperfusion injury in rat, which is exhibited by vitexin, may be related to its antioxidative and anti-inflammatory effects by regulating inflammatory cytokines and the MAPK pathway.
Department of Pharmacology, Anhui Medical University, Key Laboratory of Anti-Inflammatory and Immunopharmacology of Ministry of Education, Key Laboratory of Chinese Medicine Research and Development of State Administration of Traditional Chinese Medicine, Hefei 230032, China.
Liu-Yi
LY
Dong
Sheng
S
Li
Yi-Lan
YL
Zhen
Ya-Nan
YN
Wang
Xu
X
Shao
Zhi-Gang
ZG
Luo
D000818:Animals; D047310:Apigenin / Q000008:administration & dosage* / Q000494:pharmacology*; D002316:Cardiotonic Agents; D016207:Cytokines / Q000378:metabolism*; D004195:Disease Models, Animal; D015536:Down-Regulation; D004562:Electrocardiography; D015870:Gene Expression / Q000187:drug effects; D018836:Inflammation Mediators / Q000378:metabolism*; D007262:Infusions, Intravenous; D020935:MAP Kinase Signaling System / Q000187:drug effects* / Q000235:genetics*; D008297:Male; D017202:Myocardial Ischemia / Q000175:diagnosis* / Q000188:drug therapy* / Q000235:genetics / Q000473:pathology; D015428:Myocardial Reperfusion Injury / Q000175:diagnosis* / Q000188:drug therapy* / Q000235:genetics / Q000473:pathology; D008517:Phytotherapy; D016755:Proto-Oncogene Proteins c-jun / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D051996:Transcription Factor RelA / Q000235:genetics / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism; D015854:Up-Regulation
D002316:Cardiotonic Agents; D016207:Cytokines; D018836:Inflammation Mediators; D016755:Proto-Oncogene Proteins c-jun; D051996:Transcription Factor RelA; D014409:Tumor Necrosis Factor-alpha; D047310:Apigenin; C032731:vitexin