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芥子酸可保护心脏免受缺血/再灌注损伤,并保护H9c2心肌母细胞免受氧化应激。

Sinapic acid protects heart against ischemia/reperfusion injury and H9c2 cardiomyoblast cells against oxidative stress.

作者信息

Silambarasan Thangarasu, Manivannan Jeganathan, Priya Mani Krishna, Suganya Natarajan, Chatterjee Suvro, Raja Boobalan

机构信息

Cardiovascular Biology Lab, Department of Biochemistry and Biotechnology, Faculty of Science, Annamalai University, Tamil Nadu, India.

Cardiovascular Biology Lab, Department of Biochemistry and Biotechnology, Faculty of Science, Annamalai University, Tamil Nadu, India; Vascular Biology Lab, AU-KBC Research Centre, Anna University, Chennai, Tamil Nadu, India.

出版信息

Biochem Biophys Res Commun. 2015 Jan 24;456(4):853-9. doi: 10.1016/j.bbrc.2014.12.022. Epub 2014 Dec 13.

Abstract

The present study was designed to evaluate antioxidant and cardioprotective potential of sinapic acid (SA) against ischemia/reperfusion (I/R) injury. Cardiac functional recovery after I/R was evaluated by percentage rate pressure product (%RPP) and percentage coronary flow (%CF). Myocardial injury was evaluated by 2,3,5-triphenyltetrazolium chloride (TTC) staining and LDH enzyme leakage. Oxidative stress was estimated by lipid peroxidation level. eNOS protein expression in reperfused heart was assessed using Western blot method. Finally, in order to support the antioxidant effect of SA, in vitro protective potential of SA was assessed on H2O2-induced oxidative stress in H9c2 cardiomyoblast cells. The overall results demonstrated that I/R induced cardiac dysfunction, injury and oxidative stress was attenuated by SA treatment. Moreover, in vitro results also shown that, SA protects H9c2 cells from oxidative stress and modulates mitochondrial membrane permeability transition (MPT). In conclusion, coupled results from both in vivo and in vitro experiments have confirmed that SA with antioxidant role protects cardiac cells and its functions from I/R induced oxidative stress.

摘要

本研究旨在评估芥子酸(SA)对缺血/再灌注(I/R)损伤的抗氧化和心脏保护潜力。通过心率血压乘积百分比(%RPP)和冠脉血流百分比(%CF)评估I/R后的心脏功能恢复情况。通过氯化三苯基四氮唑(TTC)染色和乳酸脱氢酶(LDH)酶泄漏评估心肌损伤。通过脂质过氧化水平估计氧化应激。使用蛋白质印迹法评估再灌注心脏中内皮型一氧化氮合酶(eNOS)蛋白表达。最后,为了支持SA的抗氧化作用,评估了SA对H2O2诱导的H9c2心肌成纤维细胞氧化应激的体外保护潜力。总体结果表明,I/R诱导的心脏功能障碍、损伤和氧化应激通过SA治疗得到减轻。此外,体外实验结果还表明,SA保护H9c2细胞免受氧化应激并调节线粒体膜通透性转换(MPT)。总之,体内和体外实验的联合结果证实,具有抗氧化作用的SA保护心脏细胞及其功能免受I/R诱导的氧化应激。

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