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目的 :探讨抗肝昏肠液治疗肝性脑病 (HE)的作用及机制。方法 :采用药物诱导加结扎、切除 2 / 3肝脏的方法建立大鼠 HE模型 ,用抗肝昏肠液大、小剂量 (含生药 2 1.6、10 .8g/ kg)为治疗组 ,乳果糖 (3.2 6 g/ kg)为对照组 ,观察对 HE大鼠脑电图、血氨 (BA)、肿瘤坏死因子 - α(TNF- α)、白细胞介素 - 6 (IL- 6 )、肝功能及肝脏病理等的影响。结果 :抗肝昏肠液大、小剂量对上述指标都有不同程度的改善 (P <0 .0 5 ,<0 .0 1) ,尤以大剂量组为显著 ,疗效优于乳果糖 (P <0 .0 1)。结论 :抗肝昏肠液有显著的抗 HE作用 ,其机制可能为 :1阻断肠道对 BA、内毒素等有害物质的吸收 ,促进其排泄 ;2降低 TNF- α、IL- 6水平 ,阻止其对肝细胞的直接和间接损伤 ,恢复肝功能 ;3通过泻下 ,促进脑水肿消退 ;4抗菌、预防肠道细菌移行感染 ,降低感染发生率。
Objective: To explore the effect and mechanism of anti-hepatic steatorrhea in treatment of hepatic encephalopathy (HE). METHODS: Rat HE model was induced by drug-induced ligation and removal of 2 / 3 livers. The large and small doses (including crude drug 21.6, 10 .8 g / kg) of the anti-hepatic faint fluid were used as the treatment group. Lactulose (3.2) 6 g/kg) was the control group. The electroencephalogram, blood ammonia (BA), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), liver function and liver were observed in HE rats. Pathological effects. RESULTS: Large and small doses of anti-hepatic steatorrhea improved the above indexes to varying degrees (P < 0.05, <0. 01), especially in large-dose group, and the curative effect was better than that of lactulose (P < 0 .0 1). Conclusion: The anti-hepatic faecal fluid has significant anti-HE effects. The mechanism may be as follows: (1) Block intestinal absorption of harmful substances such as BA and endotoxin and promote its excretion; (2) Decrease the levels of TNF-α and IL-6 and prevent Its direct and indirect damage to liver cells, restore liver function; 3 through diarrhea, promote brain edema subside; 4 antibacterial, prevention of intestinal bacterial migration infection, reduce the incidence of infection.