Annapurna Akula, Mudagal Manjunatha P, Ansari Asif, Rao A Srinivasa
University College of Pharmaceutical Sciences, Andhra University, Vishakhapatnam, India.
Exp Clin Cardiol. 2012 Sep;17(3):110-4.
There is a comprehensive body of experimental and clinical evidence suggesting that exogenous supplementation of natural antioxidants or augmentation of endogenous antioxidants attenuates the damage caused by myocardial infarction.
To evaluate the cardioprotective effects of Cl-chalcone and F-chalcone against ischemia/reperfusion (I/R)-induced myocardial infarction in rats.
Myocardial infarct size was measured using the staining agent 2,3,5-triphenyltetrazolium chloride. Malondialdehyde was measured in serum and heart tissue, and superoxide dismutase and catalase in heart tissue were measured spectrophotometrically.
I/R resulted in significant cardiac necrosis, indicated by a rise in the end products of myocardial lipid peroxidation (malondialdehydes). A loss of antioxidative enzymes (superoxide dismutase and catalase) in heart tissue was also observed in animals subjected to in vivo myocardial I/R injury.
The present study demonstrated that treatment with Cl-chalcone and F-chalcone significantly limited infarct size, partially but significantly attenuated the level of lipid peroxidation and moderated the loss of antioxidant reserves in rats subjected to 30 min coronary artery occlusion followed by a 4 h reperfusion in comparison with I/R groups.
The results of the present study suggest that chalcones have cardioprotective activity against I/R-induced myocardial infarction in rats.
有大量实验和临床证据表明,外源性补充天然抗氧化剂或增强内源性抗氧化剂可减轻心肌梗死造成的损伤。
评估氯查尔酮和氟查尔酮对大鼠缺血/再灌注(I/R)诱导的心肌梗死的心脏保护作用。
使用染色剂2,3,5-三苯基氯化四氮唑测量心肌梗死面积。测量血清和心脏组织中的丙二醛,并通过分光光度法测量心脏组织中的超氧化物歧化酶和过氧化氢酶。
I/R导致明显的心脏坏死,表现为心肌脂质过氧化终产物(丙二醛)增加。在经历体内心肌I/R损伤的动物中,还观察到心脏组织中抗氧化酶(超氧化物歧化酶和过氧化氢酶)的损失。
本研究表明,与I/R组相比,用氯查尔酮和氟查尔酮治疗可显著限制梗死面积,部分但显著减轻脂质过氧化水平,并减轻经历30分钟冠状动脉闭塞后再灌注4小时的大鼠抗氧化储备的损失。
本研究结果表明,查尔酮对大鼠I/R诱导的心肌梗死具有心脏保护活性。