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目的:观察长期、大量给予柴胡总皂苷粗提物导致大鼠肝毒性损伤程度及与氧化损伤机制的相关性。方法:按45 d毒性试验方法,给大鼠灌胃柴胡总皂苷粗提物,按柴胡总皂苷计算,高、中、低剂量组分别为100,50,10 mg.kg-1,45 d后观察一般状况,检测肝功能相关指标,检测血和肝组织内脂质代谢情况、糖代谢、胆红素(TBIL)水平和肝组织病理检查;检测血中总巯基(-SH)的量和血、肝组织内丙二醛(MDA)水平、超氧化物歧化酶(SOD)活性、谷胱甘肽(GSH)和谷胱甘肽过氧化物酶(GSH-Px)的量和活性。结果:柴胡总皂苷粗提物可导致血中丙氨酸氨基转移酶(ALT)、天门冬氨酸氨基转移酶(AST)活性增高,肝脏重量和肝体比值增大,血和肝内TG含量增加,对血中胆固醇(CHO)和肝内糖原(Gn)影响不明显,仅高剂量组对TBIL有影响;病理组织学检查可见肝细胞损伤。可导致血中总-SH的量增加;血和肝内MDA水平、GSH含量增加,SOD,GSH-Px活性下降。上述变化随剂量的增加而逐渐加重,与蒸馏水对照组比较有明显差异。结论:柴胡总皂苷粗提物可导致大鼠明显的肝毒性损伤,其损伤途径与氧化损伤机制有关。
Objective: To observe the long-term, large doses of crude extract of Bupleurum total saponins induced liver injury in rats and its correlation with the mechanism of oxidative damage. Methods: According to the method of toxicity test for 45 days, the crude extracts of Radix Bupleuri were administered to rats. According to the calculation of total saikosaponin, the rats in high, middle and low dose groups were 100, 50, 10 mg.kg-1, d, the general condition was observed, the indexes related to liver function were detected, the lipid metabolism, glucose metabolism, bilirubin (TBIL) and liver histopathological examination were detected; the amount of total sulfhydryl (-SH) And blood, malondialdehyde (MDA) level, superoxide dismutase (SOD) activity, glutathione (GSH) and glutathione peroxidase (GSH-Px) Results: The crude extract of Bupleurum sativum total saponins can lead to the increase of alanine aminotransferase (ALT), aspartate aminotransferase (AST) activity, the increase of liver weight and ratio of liver, blood and liver TG (CHO) and hepatic glycogen (Gn) in serum were not obvious, only high dose group had effect on TBIL, and pathological examination showed hepatocyte injury. Can lead to an increase in the amount of blood total-SH; blood and liver MDA levels, GSH content increased, SOD, GSH-Px activity decreased. The above changes gradually increased with the increase of dose, compared with the distilled water control group there are significant differences. Conclusion: The crude extract of Bupleurum saponins can cause obvious hepatotoxic injury in rats, and its damage pathway is related to the mechanism of oxidative damage.