论文部分内容阅读
目的:研究四逆汤(Sini decoction,SND)对脓毒症模型大鼠心肌细胞线粒体损伤的保护机理。方法:将70只大鼠随机分为正常对照组10只,模型组和四逆汤组各30只,(1、3、5 d各10只),通过失血以及静脉注射脂多糖2次打击以建立脓毒症大鼠模型。四逆汤组在二次打击后给予四逆汤灌胃,1次/d;模型组按相同溶液体质量剂量、时点灌蒸馏水。在模型建立后的1、3、5 d分别处死大鼠,采血行心脏有关酶学CK、CK-MB检测;分离心肌细胞线粒体,行线粒体肿胀度、膜电位及总ATP酶、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GPx)检测;电镜观察心肌细胞线粒体形态学变化。结果:与正常对照组比较,模型组CK、CK-MB及线粒体肿胀度显著升高(P<0.01),1 d时出现峰值,而治疗组较模型组有显著改善(P<0.01)。模型组的线粒体膜电位、总ATP酶、SOD及GSH值与正常对照组比较显著降低(P<0.01),而治疗组较模型组显著(P<0.05或P<0.01)。电镜观察脓毒症模型组线粒体结构破坏明显,出现空泡化,而治疗组较模型组减轻。结论:四逆汤能有效保护脓毒症心肌细胞线粒体功能,其机制可能与提高线粒体的抗氧化能力、减少氧化损伤、改善线粒体的呼吸功能有关。
Objective: To investigate the protective mechanism of Sini decoction (SND) on mitochondrial damage of myocardial cells in septic rats. Methods: Seventy rats were randomly divided into normal control group (n = 10), model group (n = 30) and Sini Decoction group (n = 30). The rats were sacrificed by blood loss and intravenous injection of lipopolysaccharide Establishment of septic rat model. Sini Decoction group was given after the second attack Sini Decoction intragastric administration, 1 / d; model group at the same solution body mass dose, point irrigation distilled water. The rats were sacrificed on the 1st, 3rd, 5th day after model establishment. Blood samples were collected for cardiomyocyte CK and CK-MB detection. Myocardial mitochondria were isolated and mitochondria swelling, membrane potential, total ATPase and superoxide dismutase Enzyme (SOD) and glutathione peroxidase (GPx) were detected. The morphological changes of mitochondria in myocardial cells were observed by electron microscope. Results: Compared with the normal control group, the CK, CK-MB and mitochondrial swelling in the model group were significantly increased (P <0.01), and peaked at the first day. The treatment group was significantly improved compared with the model group (P <0.01). The mitochondrial membrane potential, total ATPase, SOD and GSH in the model group were significantly lower than those in the normal control group (P <0.01), while those in the untreated group were significantly higher than those in the untreated group (P <0.05 or P <0.01). Electron microscopy of sepsis model group mitochondrial structure damage significantly, there vacuolization, while the treatment group than the model group. Conclusion: Sini Decoction can effectively protect mitochondrial function of septic cardiomyocytes, and its mechanism may be related to improving mitochondrial antioxidant capacity, reducing oxidative damage and improving mitochondrial respiratory function.