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复方甘草酸苷对大鼠急性肝衰竭保护机制的研究

     

摘要

Objective To study the protective mechanism of compound glycynrhizin ( CG) on acute hepatic failure (AHF) in rats. Methods 90 rats were randomly divided into normal group,model group and treatment group (compound glycyrrhizin). Thioacetamide (TAA) 600 mg/kg was given (iv. ) once daily for 2 times,and model of AHF was made. Treatment group was given CG 2 mL/100 g (iv. ) at 3 d before and after treatment besides TAA, while control group and AHF group were given NS 1 mL/100 g ( ih. ). The ALT, TBIL, PTA, endotoxin and many kinds of inflammatory factor level were measured. The hepatic tissue was taken and fixed into 10% formalin after 2 weeks, and the masccline rate of proliferation cell nuclear antigen was detected. Results Compared with AHF group and control group,serum ALT levels in treatment group were significantly lower (P <0. 01) ;The average level of serum total bilirubin (TBIL) in treatment group was lower,and the average level of serum plasma prothrombin activity ( PTA) was higher after 2 weeks ( P < 0. 01) ; The level of TNF-a in treatment group was lower during treatment (P < 0. 01). The levels of plasma endotoxin and interleukin-6 in treatment group were significantly lower after 2 weeks (P < 0. 01). The masccline rate of proliferation cell nuclear antigen in treatment group was higher than those of control group after 2 weeks ( P < 0. 01) . Conclusion CG can protect AHL of rat model, and the mechanism could be concerned with decreasing levels of endotoxin and cytokine, promoting express of proliferation cell nuclear antigen.%目的 探讨甘草酸苷对大鼠急性肝衰竭(AHF)的保护机制.方法 将90只Wistar大鼠随机分为3组:正常对照组(对照组)、模型组(AHF组)、治疗组(甘草酸苷组),静脉注射硫代乙酰胺(TAA )600 mg/kg,2次,每次间隔24 h,复制AHF动物模型.治疗组动物除予TAA外,于实验前3d至实验结束分别静滴甘草酸苷注射液2 mL/100 g,对照组和AHF组同时皮下注射0.9%氯化钠液1 mL/100 g.AHF组、治疗组于第2次注射TAA后24h,随机各取8只,治疗中分时段取大鼠腹主动脉血检测肝功能、PTA、血清内毒素及多种炎性因子水平.2周后,取肝组织,用10%甲醛液固定,检测肝细胞增殖细胞核抗原阳性率(PCNA).结果 与AHF组、对照组相比,治疗中,治疗组血清ALT水平降低(P<0.01);治疗2周后,治疗组血清总胆红素水平(同比例)降低,而血浆凝血酶原活动度(PTA)均值较高(P<0.01);治疗后各时相点,治疗组TNF-α水平较低(P<0.01);治疗2周后,治疗组患者血浆内毒素及IL-6水平显著降低(P<0.01).治疗2周后,治疗组PCNA阳性细胞表达显著高于对照组(P<0.01).结论 甘草酸苷对急性肝衰竭大鼠模型具有保护作用,其机制可能与降低血浆内毒素及细胞因子水平、促进肝组织PCNA表达有关.

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