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目的 :观察中药复方四毒清对LPS引起的心肌损伤以及心肌TNFα和自由基生成的影响 ,探讨四毒清防治内毒素性心功能障碍的机制。方法 :将小鼠随机分成 4组 :对照组、LPS组、四毒清防治组和四毒清组 ,分别用蒸馏水和四毒清 (0 2mL/10g)灌胃 3d ,每天 2次 ,最后 1次灌胃后 2h ,腹腔注射LPS(30mg/kg)或生理盐水 (0 2mL/10g)。测定小鼠血浆肌酸激酶 (CK)、心肌超氧化物歧化酶 (SOD)的活性以及心肌TNFα和丙二醛 (MDA)的含量 ,并观察心肌组织结构和超微结构的改变。结果 :LPS注射后 12h和 2 4h ,小鼠心肌组织出现明显水肿 ,肌原纤维肿胀、排列稀疏 ,心肌间质可见少数红细胞 ;电镜观察显示 ,心肌细胞核皱缩、染色质边集 ,部分肌丝断裂 ,线粒体肿胀。四毒清防治组小鼠心肌病理改变明显轻于LPS组 ;LPS组小鼠血浆CK的活性和心肌TNFα含量明显高于对照组和四毒清防治组 ,心肌SOD活性明显低于四毒清防治组 ,而心肌MDA的含量没有显著差别 ;四毒清组和对照组比较 ,除心肌MDA含量外 ,上述其它指标没有明显差别。结论 :四毒清能减轻内毒素诱导的心肌损伤 ,其机制可能与四毒清抑制心肌TNFα生成有关
Objective : To observe the effect of Siduqing, a traditional Chinese medicine compound, on the myocardial damage induced by LPS and the production of myocardial TNFα and free radicals, and to explore the mechanism of Siduqing in preventing and treating endotoxin-induced cardiac dysfunction. METHODS: Mice were randomly divided into 4 groups: control group, LPS group, Siduqing prevention group and Siduqing group. The rats were treated with distilled water and Siduqing (0 2 mL/10g) for 3 days, twice daily, and finally 1 Two hours after the second gavage, LPS (30 mg/kg) or physiological saline (0 2 mL/10 g) was intraperitoneally injected. The activity of creatine kinase (CK), myocardial superoxide dismutase (SOD) and myocardial TNFα and malondialdehyde (MDA) in mice were measured, and the changes of myocardial structure and ultrastructure were observed. RESULTS: At 12h and 24h after LPS injection, myocardium showed marked edema, myofibrils swollen and sparsely arranged, and a few red blood cells were observed in the interstitial of myocardium. Electron microscopy showed that the myocardial cell nuclei were shrinking, chromatin margins, and some myofilaments Broken, mitochondria swollen. The myocardial pathological changes in mice treated with Siduqing were significantly lighter than those in LPS group; the activity of plasma CK and the content of myocardial TNFα in mice of LPS group were significantly higher than those in the control group and Siduqing prevention group. The activity of SOD in myocardial tissue was significantly lower than that of Siduqing There was no significant difference in the content of MDA in the myocardium. Compared with the control group, there was no significant difference in the content of MDA between myocardium and the control group. Conclusion : Si Duo Qing can reduce endotoxin-induced myocardial injury and its mechanism may be related to the inhibition of myocardial TNF-α production by Si Duo Qing