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目的观察当归多糖(Angelica sinensis polysaccharides,ASP)对四氯化碳性肝硬化大鼠肝性脑病发生的预防作用,并探讨其机制。方法400ml/L四氯化碳皮下注射造模,分别给予蒸馏水(阴性组),乳果糖(50g∶100ml,阳性药物组),ASP10、20、40g/L溶液10ml.kg-1.d-1灌胃,连续14d后用内毒素(3mg/kg)诱导大鼠昏迷,观察注射内毒素后12h内各组大鼠昏迷发生时间和数量,测定各组大鼠的血氨、血清谷丙转氨酶(GPT)、谷草转氨酶(GOT)浓度,观察脑细胞凋亡情况和星形胶质细胞数量。结果各组大鼠血氨、GPT、GOT水平,脑细胞凋亡数和昏迷率,阴性组最高;ASP40g/L组的血氨、GOT水平和昏迷率均低于阳性药物组,ASP3个剂量组的脑细胞凋亡数均低于阳性药物组,而星形胶质细胞数阴性组最低,且ASP3个剂量组均高于阳性药物组。结论ASP可保护脑功能,减缓肝性脑病的发生,作用优于阳性药物乳果糖。其机制可能与降低血氨,改善肝功能,保存星形胶质细胞和神经元的活性有关。
Objective To observe the preventive effect of angelica sinensis polysaccharides (ASP) on hepatic encephalopathy in rats with carbon tetrachloride-induced cirrhosis and to explore the mechanism. Methods 400ml/L carbon tetrachloride was injected subcutaneously and given distilled water (negative group), lactulose (50g: 100ml, positive drug group), ASP10, 20, 40g/L solution 10ml.kg-1.d-1 After intragastric administration for 14 days, rats were induced to coma by endotoxin (3 mg/kg). The time and number of coma in rats in each group were observed within 12 hours after endotoxin injection. Blood ammonia and serum glutamic-pyruvic transaminase were measured in rats in each group. GPT) and aspartate aminotransferase (GOT) concentrations were used to observe the apoptosis of brain cells and the number of astrocytes. Results Blood ammonia, GPT, GOT levels, brain cell apoptosis and coma rate in each group were highest in the negative group; ammonia, GOT levels, and coma rates in the ASP40g/L group were lower than those in the positive group, and ASP3 dose groups. The number of apoptotic cells in the brain was lower than that in the positive drug group, while the number of astrocytes in the negative group was the lowest, and the ASP3 dose group was higher than the positive drug group. Conclusion ASP can protect brain function and reduce the occurrence of hepatic encephalopathy. The effect of ASP is better than that of the positive drug lactulose. The mechanism may be related to reducing blood ammonia, improving liver function, and preserving the activity of astrocytes and neurons.