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目的研究川芎嗪(TMP)对脓毒症大鼠肝细胞线粒体结构的保护作用及可能机制。方法实验大鼠被分成对照组、脓毒症组、治疗组和预防组;用盲肠结扎穿孔法制备大鼠脓毒症实验模型,在术后10 h,取肝脏标本用JEM-1230透射电子显微镜观察肝细胞的超微结构,选用Image-Pro Plus 6.0图像软件对线粒体进行测量;用Western blot技术检测肝细胞线粒体内膜水通道蛋白(AQP)8的表达。结果和对照组比较,其余3组单个肝细胞切面的线粒体总数和数密度均减少(P<0.01),但治疗组和预防组均多于脓毒症组(P<0.01);线粒体体积密度脓毒症组也较对照组低(P<0.01);线粒体内膜AQP8的相对表达量在脓毒症组、治疗组和预防组均较对照组明显减少(P<0.01);治疗组和预防组的AQP8相对表达量较脓毒症组增多(P<0.01)。结论在脓毒症状态下,TMP可保护肝细胞线粒体的结构,可能是通过增加线粒体内膜AQP8表达而起作用的。
Objective To investigate the protective effect of ligustrazine (TMP) on the mitochondrial structure of hepatocytes in septic rats and its possible mechanism. Methods The experimental rats were divided into control group, sepsis group, treatment group and prophylaxis group. Experimental rat model of sepsis was established by cecal ligation and perforation method. At 10 h after operation, the liver samples were taken by using JEM-1230 transmission electron microscope The ultrastructure of hepatocytes was observed. Image-Pro Plus 6.0 software was used to measure mitochondria. Western blot was used to detect the expression of aquaporin 8 (AQP) in hepatocytes. Results Compared with the control group, the mitochondrial counts and number densities of the other three groups were decreased (P <0.01), but the treatment group and the prevention group were more than those of the sepsis group (P <0.01); mitochondrial bulk density pus Compared with the control group, the expression of AQP8 in mitochondrial membrane was significantly decreased in the sepsis group, the treatment group and the prophylaxis group (P <0.01) The relative expression of AQP8 in sepsis group increased (P <0.01). Conclusion TMP protects the mitochondrial structure of hepatocytes in sepsis state, which may play an important role in increasing mitochondrial AQP8 expression.