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目的:观察血必净注射液对脓毒症大鼠早期血浆总蛋白(TP)、白蛋白(ALB)水平的影响,拟从分子生物学角度阐明可能存在的机制。方法:54只健康雄性Wistar大鼠随机分为正常对照组、脓毒症组和血必净治疗组,尾静脉注射脂多糖(lipopolysaccharide,LPS)建立脓毒症模型。各组在建立模型后6,12,24 h作为观察点,测量各组的血浆总蛋白、白蛋白值;采用Western blot法对3组大鼠肝脏AMPK,eEF2蛋白进行检测。结果:与正常对照组比较,LPS尾静脉注射6,12 h后,脓毒症组、血必净组的TP及ALB尚无变化;但24 h后脓毒症组TP和ALB明显低于正常组(P<0.01),pho-AMPK,pho-eEF2在肝脏的表达也相应增加(P<0.01),而血必净组无明显变化;各组间总AMPK,eEF2均无统计学差异。与脓毒症组比较,血必净治疗组24 h TP,ALB明显升高(P<0.05),但稍低于对照组;血必净组pho-AMPK,pho-eEF2在肝脏的表达明显下降(P<0.05)。结论:脓毒症早期应用血必净注射液可以通过AMPK途径抑制肝脏蛋白的分解,减少血浆蛋白的分解。
Objective: To observe the effect of Xuebijing injection on plasma total protein (TP) and albumin (ALB) in early stage of septic rats, and to elucidate the possible mechanism from the perspective of molecular biology. Methods: Fifty - four healthy male Wistar rats were randomly divided into normal control group, sepsis group and Xuebijing group, and lipopolysaccharide (LPS) was injected into tail vein to establish a sepsis model. The rats in each group were taken as observation points 6, 12 and 24 hours after establishment of the model to measure the total protein and albumin in each group. Western blot was used to detect the protein levels of AMPK and eEF2 in the three groups. Results: Compared with the normal control group, TP and ALB in sepsis group and Xuebijing group did not change after 6 and 12 h of tail vein injection of LPS, but TP and ALB in sepsis group were significantly lower than normal after 24 h (P <0.01). The expression of pho-AMPK and pho-eEF2 also increased in the liver (P <0.01), but there was no significant change in Xuebijing group. There was no significant difference in total AMPK and eEF2 among the groups. Compared with the sepsis group, the serum levels of TP and ALB in Xuebijing group were significantly increased at 24 h (P <0.05), but slightly lower than those in the control group; the expression of pho-AMPK and pho-eEF2 in Xuebijing group was significantly decreased (P <0.05). Conclusion: The application of Xuebijing injection in early sepsis can inhibit the decomposition of liver protein through the AMPK pathway and reduce the breakdown of plasma proteins.