Rao Pragada Rajeswara, Viswanath Routhu Kasi
Department of Pharmacology, University College of Pharmaceutical Sciences, Andhra University, Andhra Pradesh, India.
Exp Clin Cardiol. 2007 Winter;12(4):179-87.
There is comprehensive experimental and clinical evidence that either exogenous supplementation of natural antioxidants or augmentation of endogenous antioxidants attenuates myocardial infarction.
To investigate the effects of chronic administration of silymarin against ischemia-reperfusion-induced myocardial infarction in rats.
Silymarin was administered orally to Wistar albino rats (200 g to 250 g) in three different doses (100 mg/kg, 250 mg/kg and 500 mg/kg), by gastric gavage for one week. At the end of this period, control (ischemia-reperfusion) groups and silymarin-treated groups were subjected to 30 min occlusion of the left anterior descending coronary artery and thereafter reperfused for 4 h.
Ischemia-reperfusion resulted in significant cardiac necrosis, indicated by elevated levels of serum marker enzymes such as serum glutamate oxaloacetate transaminase, serum glutamate pyruvate transaminase, lactate dehydrogenase, creatine kinase-isoenzyme and creatine kinase. A significant rise in the end products of myocardial lipid peroxides (malondialdehydes [MDAs]), loss of antioxidative enzymes (superoxide dismutase, catalase, glutathione S-transferase and reduced glutathione) and increased levels of myeloperoxidase in heart tissue were observed in the animals subjected to in vivo myocardial ischemia-reperfusion injury. Infarct size was measured by using the staining agent 2,3,5-triphenyltetrazolium chloride. A lead II electrocardiogram was monitored at various intervals throughout the experiment.
The present study showed that silymarin protected the endogenous antioxidant enzymes, suppressed the neutrophil infiltration during ischemia-reperfusion and limited the infarct size, with concomitant reduction in serum MDA, tissue MDA and serum marker enzymes in rats subjected to 30 min coronary artery occlusion followed by 4 h of reperfusion. Pretreatment with silymarin also protected rat hearts from a further drop in mean arterial blood pressure during reperfusion, and restored heart rate at the end of the reperfusion period.
The present study suggests that the phytochemical silymarin has cardioprotective activity against ischemia-reperfusion-induced myocardial infarction in rats.
有全面的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均可减轻心肌梗死。
研究长期给予水飞蓟宾对大鼠缺血再灌注诱导的心肌梗死的影响。
将水飞蓟宾以三种不同剂量(100mg/kg、250mg/kg和500mg/kg)经胃管口服给予体重200g至250g的Wistar白化大鼠,持续一周。在此期间结束时,对对照组(缺血再灌注组)和水飞蓟宾处理组进行左前降支冠状动脉闭塞30分钟,然后再灌注4小时。
缺血再灌注导致明显的心肌坏死,表现为血清标志物酶如血清谷草转氨酶、血清谷丙转氨酶、乳酸脱氢酶、肌酸激酶同工酶和肌酸激酶水平升高。在经历体内心肌缺血再灌注损伤的动物中,观察到心肌脂质过氧化物(丙二醛[MDA])终产物显著增加、抗氧化酶(超氧化物歧化酶、过氧化氢酶、谷胱甘肽S -转移酶和还原型谷胱甘肽)丧失以及心脏组织中髓过氧化物酶水平升高。梗死面积通过使用染色剂2,3,5 -三苯基氯化四氮唑进行测量。在整个实验过程中,每隔一段时间监测II导联心电图。
本研究表明,水飞蓟宾可保护内源性抗氧化酶,抑制缺血再灌注期间的中性粒细胞浸润并限制梗死面积,同时使经历30分钟冠状动脉闭塞随后4小时再灌注的大鼠血清MDA、组织MDA和血清标志物酶水平降低。水飞蓟宾预处理还可保护大鼠心脏在再灌注期间平均动脉血压不再进一步下降,并在再灌注期结束时恢复心率。
本研究表明,植物化学物质水飞蓟宾对大鼠缺血再灌注诱导的心肌梗死具有心脏保护活性。