目的 研究红芪多糖对CCl₄致小鼠肝纤维化及骨丢失的防治作用,同时探讨肝纤维化对骨丢失的影响。方法 以sc 40% CCl₄的橄榄油溶液(0.1 mL/kg,5 d一次,连续7次)制备小鼠肝纤维化模型,同时给予高、中、低剂量红芪多糖(20、10、5 g/kg)及秋水仙碱(0.6 mg/kg),连续35 d后,试剂盒法测定血清中丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)、总蛋白(TP)、白蛋白(ALB)水平,计算白球比例(A/G);检测肝脏及胸腺指数;取肝脏进行组织病理学观察。测定骨丢失指标,试剂盒法检测血清中抗酒石酸酸性磷酸酶(TRACP)、碱性磷酸酶(ALP)、Ca、P水平,骨中羟脯氨酸(Hyp)水平。结果 与对照组比较,模型组血清中ALT、AST、TP水平显著升高,ALB、A/G显著降低;组织学切片呈现明显的病理变化;肝脏指数和胸腺指数明显上升;骨丢失指标中,血清TRACP、ALP、Ca、P水平明显上升,骨中Hyp水平明显降低;红芪多糖能显著改善CCl₄所致小鼠肝纤维化及骨丢失的状况。结论 CCl₄造成小鼠肝纤维化的同时引起骨丢失,肝纤维化是导致骨丢失的原发性病因;红芪多糖对CCl₄造成小鼠肝纤维化具有明显改善作用,对肝纤维化引起的骨丢失也有显著影响。

Objective To investigate the protective effect of Hedysari Radix polysaccharide (HRP) on liver fibrosis in mice and the correlation between the hepatic fibrosis and bone loss. Methods The mice were sc injected with 40% carbon tetrachloride (CCl₄) dissolved in olive oil solution (0.1 mL/kg, once every 5 days ), while given high-, mid-, and low-dose (20, 10, and 5 g crude drug/kg) HRP and colchicines (0.6 mg/kg) daily. Continuous 35 d later, the activity of alanine transarninase (ALT) and aspartate transferase (AST), contents of total protein (TP) and albumin (ALB) were investigated by related reagent kit, and then, calculated the albumin/globulin (A/G) ratio, liver and thymus indexes and liver histological of tissue pathology were determined. The serum level of acid phosphatase resistant to acid phosphatase (TRACP), alkaline phosphatase (ALP), Ca, P, and the bone level of hydroxyproline (Hyp) were investigated by related reagent kit to observe bone loss. Results The model group compared with the Sham group, the levels of ALT, AST, and TP increase, showed obvious liver pathological damage, liver and thymus index increase, levels of TRACP, ALP, Ca, and P decrease, and Hyp increase. HRP could significantly improve the hepatic fibrosis and bone loss induced by CCl₄ in mice. Conclusion The liver fibrosis in mice could also cause bone loss and be the primary cause of bone loss in this experiment. The certain market value of this Chinese materia medica is developed for its significant effect and contact between hepatic fibrosis and bone loss is initially investigated, which lays the foundation to further discuss the mechanism of the above two.

甘肃省科技支撑项目(1304FKCA101)