Karunakaran Gauthaman
Department of Pharmacology, College of Pharmacy, King Khalid University, Abha 61441, Kingdom of Saudi Arabia.
Anc Sci Life. 2015 Oct-Dec;35(2):79-84. doi: 10.4103/0257-7941.171674.
The present study was designed to investigate the cardio protective role of chronic oral administration of methanolic extract of Terminalia arjuna bark in in-vitro myocardial ischemic reperfusion injury and the induction of HSP72.
Rats, divided into three groups, and were administered with the methanolic extract of the bark powder of Terminalia arjuna (TAME) by oral gavage (6.75 and 9.75 mg/kg: 6 days/week for 12 weeks). Control and TAME extract treated rat hearts were subjected to in-vitro global ischemic reperfusion injury (5 min perfusion, 9 min noflow and 12 min reperfusion).
Oxidative stress in MIRI was evidenced by, raised levels of myocardial TBARS and depletion of endogenous myocardial antioxidants GSH, SOD and catalase. Western blot analysis showed a single band corresponding to 72 kDa in homogenates of hearts from rat treated with both the doses. In the methanolic extract of the bark powder of Terminalia arjuna treatment groups, both the doses had better recovery of myocardial function, with significant reduction in TBARS, and rise in SOD, GSH, catalase were observed.
The results of the present study suggest that the methanolic extract of the bark powder of Terminalia arjuna in rat induces myocardial HSP72 and augments myocardial endogenous antioxidants, without causing any cellular injury and offers better cardioprotection against oxidative stress associated with myocardial IR injury.
本研究旨在探讨长期口服阿育王榄仁树皮甲醇提取物对体外心肌缺血再灌注损伤及热休克蛋白72(HSP72)诱导的心脏保护作用。
将大鼠分为三组,通过灌胃给予阿育王榄仁树皮粉末甲醇提取物(TAME,6.75和9.75毫克/千克,每周6天,共12周)。对对照组和TAME提取物处理的大鼠心脏进行体外全心缺血再灌注损伤(5分钟灌注、9分钟无血流和12分钟再灌注)。
心肌缺血再灌注损伤中的氧化应激表现为心肌丙二醛(TBARS)水平升高以及内源性心肌抗氧化剂谷胱甘肽(GSH)、超氧化物歧化酶(SOD)和过氧化氢酶的消耗。蛋白质免疫印迹分析显示,两个剂量处理的大鼠心脏匀浆中均出现一条对应72 kDa的条带。在阿育王榄仁树皮粉末甲醇提取物处理组中,两个剂量均使心肌功能恢复更好,TBARS显著降低,SOD、GSH、过氧化氢酶水平升高。
本研究结果表明,阿育王榄仁树皮粉末甲醇提取物在大鼠中可诱导心肌HSP72并增强心肌内源性抗氧化剂,且不会造成任何细胞损伤,并对与心肌缺血再灌注损伤相关的氧化应激提供更好的心脏保护作用。