文章摘要
秦 军,初晓倩,李庆平.TG-6对大鼠心肌缺血再灌注损伤的保护作用及其机制研究[J].南京医科大学学报,2016,(8):912~916
TG-6对大鼠心肌缺血再灌注损伤的保护作用及其机制研究
Protective effects of TG-6 on myocardial ischemia-reperfusion injury and its mechanism
投稿时间:2016-01-03  
DOI:10.7655/NYDXBNS20160803
中文关键词: TG-6  心肌缺血再灌注损伤  炎症  氧化应激
英文关键词: TG-6  myocardial ischemia-reperfusion injury  inflammation  oxidative stress
基金项目:国家自然科学基金(30973534,81173052);南京医科大学科技发展基金(2013NJMU004)
作者单位
秦 军 南京医科大学药理学系,江苏 南京 211166 
初晓倩 南京医科大学药理学系,江苏 南京 211166 
李庆平 南京医科大学药理学系,江苏 南京 211166 
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中文摘要:
      目的:研究新化合物 TG-6 对大鼠心肌缺血再灌注(myocardial ischemia reperfusion,I/R)损伤的保护作用及其机制?方法:大鼠于I/R 前 5 min 尾静脉注射药物,结扎大鼠左冠状动脉前降支缺血45 min,再灌注24 h后,测定大鼠心电图,心肌组织HE染色观察其病理学变化;测定血清中乳酸脱氢酶(lactate dehydrogenase,LDH)?肌酸激酶(creatine kinase,CK)?超氧化物歧化酶(superoxide dismutase,SOD)?丙二醛(malondialdehyde,MDA)等含量;检测血清中炎症因子,如肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)?白介素-6(interleukin-6,IL-6)?白介素-1β(interleukin-1β,IL-1β)含量,Western blot测定TLR4?IκBα?NF-κB蛋白的表达?结果:与模型组相比,TG-6可以明显改善心电图S-T段的抬高,减轻心肌组织梗死面积和病理损伤,显著降低血清中LDH?CK?MDA?TNF-α?IL-6和IL-1β的含量,增加SOD活性?TG-6能减少心肌组织中TLR4?IκBα?NF-κB蛋白的表达?结论:TG-6对心肌缺血再灌注损伤具有保护作用,其机制可能与抗炎和抗氧化有关?
英文摘要:
      Objective:To investigate the effect of TG-6 on myocardial ischemia reperfusion injury in rats and the underlying mechanism. Methods:The drugs were administered by intravenous injection 5 min before ischemia reperfusion(I/R)injury. Myocardial ischemia reperfusion injury(MI/RI)model was treated by 45 min of left anterior descending(LAD)occlusion followed by 24 h of reperfusion. Measurement of rat electrocardiogram(ECG),hematoxylin-eosin(HE)staining of cardiac tissue,serum lactate dehydrogenase(LDH),creatine kinase(CK),superoxide dismutase(SOD)and malondialdehyde(MDA). Serum inflammatory cytokines,such as tumor necrosis factor-α(TNF-α),interleukin-6(IL-6)and interleukin -1β(IL-1β)were measured by ELISA kits. The protein expression of TLR4,IκBα and NF-κB were measured by Western blot. Results:Compared with the I/R group,TG-6 decreased S-T elevation,reduced myocardial pathological lesions,significantly decreased serum LDH,CK,MDA,TNF-α,IL-6,IL-1β content,and increased SOD activity. TG-6 reduced TLR4,IκBα and NF-κB protein expression in cardiac tissue. Conclusion:TG-6 exerts strong favorable cardioprotective function on myocardial I/R injury, which may be related to anti-inflammatory and antioxidant activity.
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