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.
Am J Chin Med. 2013;41(6):1251-66. doi: 10.1142/S0192415X13500845.
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.
本研究旨在探讨牡荆素（vitexin）对大鼠心肌缺血/再灌注（I/R）损伤的心肌保护作用及其可能的作用机制。结扎大鼠前降支 30min 后再灌注 60min 建立心肌 I/R 模型，观察心电图（ECG）ST 段抬高；氯化三苯基四氮唑（TTC）染色评估大鼠心脏梗死面积；测定乳酸脱氢酶（LDH）、肌酸激酶（CK）、超氧化物歧化酶（SOD）活性和丙二醛（MDA）含量；免疫组化法检测心肌核因子-κB p65（NF-κBp65）和肿瘤坏死因子-α（TNF-α）的表达；Western blot 检测细胞外信号调节激酶（ERK）/磷酸化 ERK（phospho-ERK）和 c-Jun/磷酸化 c-Jun（phospho-c-Jun）蛋白的表达。牡荆素显著降低 ECG 中 ST 段的升高和心肌梗死面积。血清中 LDH 和 CK 活性及 MDA 含量降低，SOD 活性明显增强。牡荆素显著抑制 I/R 诱导的心肌 NF-κB 和 TNF-α的增加。此外，Western blot 分析表明，与 I/R 组相比，牡荆素显著增强了磷酸化 ERK 的表达，减弱了磷酸化 c-Jun 的表达。牡荆素对大鼠心肌缺血再灌注损伤具有显著的保护作用，可能与其通过调节炎症细胞因子和 MAPK 通路发挥抗氧化和抗炎作用有关。
