Department of Biochemistry and Biotechnology, Annamalai University, Annamalai Nagar 608002, Tamil Nadu, India.
Department of Biochemistry and Biotechnology, Annamalai University, Annamalai Nagar 608002, Tamil Nadu, India.
Chem Biol Interact. 2015 May 5;232:68-76. doi: 10.1016/j.cbi.2015.03.009. Epub 2015 Mar 17.
The present study aims to evaluate the preventive effects of vanillic acid on altered ion pumps, ions and Fas-receptor and caspase mediated apoptosis-signaling pathway and cardiomyocyte death in isoproterenol induced myocardial infarcted rats. Male albino Wistar rats were pretreated with vanillic acid (5 mg/kg and 10 mg/kg body weight) daily for 10 days. After the pretreatment, isoproterenol (100 mg/kg body weight) was injected into rats at an interval of 24h for 2 days to induce myocardial infarction. Isoproterenol induced rats significantly increased activities/levels of serum cardiac markers, plasma lipid peroxidation products, serum uric acid and significantly decreased plasma non-enzymatic antioxidants. Furthermore, isoproterenol significantly altered the activities/levels of ion pumps and ions in the heart. The myocardial expressions of apoptotic genes such as Fas-receptor, caspases-8, -9, and -3 were increased in isoproterenol induced rats. There was a significant increase in cardiomyocyte apoptosis observed in isoproterenol induced rats. Pretreatment with vanillic acid (5 mg/kg and 10 mg/kg body weight) to isoproterenol induced rats showed significant effects on all the biochemical and molecular parameters evaluated. Isolated cardiomyocyte viability by trypan blue exclusion staining also correlated with these biochemical findings. Thus, vanillic acid prevented altered ion pumps, ions and inhibited Fas-receptor and caspase mediated apoptosis-signaling pathway and cardiomyocyte death in isoproterenol induced myocardial infarcted rats. Our study also revealed that pretreatment with vanillic acid at the dose of 10 mg/kg body weight was more effective than 5 mg/kg body weight. The cardioprotective effects of vanillic acid are associated with its antioxidant mechanisms.
本研究旨在评估香草酸对异丙肾上腺素诱导心肌梗死大鼠改变的离子泵、离子和 Fas 受体及半胱氨酸蛋白酶介导的凋亡信号通路及心肌细胞死亡的预防作用。雄性白化 Wistar 大鼠每天用香草酸(5mg/kg 和 10mg/kg 体重)预处理 10 天。预处理后,异丙肾上腺素(100mg/kg 体重)以 24 小时的间隔给大鼠注射 2 天以诱导心肌梗死。异丙肾上腺素诱导的大鼠显著增加了血清心脏标志物、血浆脂质过氧化产物、血清尿酸的活性/水平,显著降低了血浆非酶抗氧化剂的活性/水平。此外,异丙肾上腺素显著改变了心脏中离子泵和离子的活性/水平。凋亡基因如 Fas 受体、半胱氨酸蛋白酶-8、-9 和 -3 的心肌表达在异丙肾上腺素诱导的大鼠中增加。异丙肾上腺素诱导的大鼠中观察到心肌细胞凋亡显著增加。用香草酸(5mg/kg 和 10mg/kg 体重)预处理异丙肾上腺素诱导的大鼠对所有评估的生化和分子参数均显示出显著效果。台盼蓝排斥染色法分离的心肌细胞活力也与这些生化发现相关。因此,香草酸可防止改变的离子泵、离子,并抑制 Fas 受体和半胱氨酸蛋白酶介导的凋亡信号通路和异丙肾上腺素诱导的心肌梗死大鼠的心肌细胞死亡。我们的研究还表明,用香草酸预处理的剂量为 10mg/kg 体重比 5mg/kg 体重更有效。香草酸的心脏保护作用与其抗氧化机制有关。