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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。
Objective: To study the protective effect of a novel compound TG-6 on myocardial ischemia reperfusion (I / R) injury in rats and its mechanism. Methods: Rats were injected intravenously with tail veins at 5 min before I / R, and the anterior descending coronary artery of rats was ligated for 45 min and reperfused for 24 h. The changes of electrocardiogram and myocardial tissue were observed by HE staining and the pathological changes were observed Serum levels of lactate dehydrogenase (LDH), creatine kinase (CK), superoxide dismutase (SOD) and malondialdehyde (MDA) Inflammatory cytokines such as tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), interleukin-1β (IL- blot was used to detect the expression of TLR4, IκBα and NF-κB. Results: Compared with the model group, TG-6 could significantly improve the elevation of ST segment of ECG, reduce myocardial infarct size and pathological damage, and significantly reduce the levels of LDH, CK, MDA, TNF-α, IL-6 and IL- 1β content, increase SOD activity. TG-6 can reduce myocardial tissue TLR4, IκBα, NF-κB protein expression. Conclusion: TG-6 has a protective effect on myocardial ischemia-reperfusion injury, and its mechanism may be related to anti-inflammation and anti-oxidation.