茵陈多糖对妊娠胆汁淤积大鼠肝脏氧化损伤的保护作用研究

Protective effect of capillary artemisia polysaccharide for liver oxidative damage rats with intrahepatic cholestasis of pregnancy

目的探讨茵陈多糖对妊娠胆汁淤积大鼠肝脏氧化损伤的保护作用。方法采用随机数字表法将32只妊娠SD大鼠分为对照组、模型组、低剂量组及高剂量组,妊娠16周除对照组外均采用苯甲酸雌二醇注射法建立妊娠胆汁淤积大鼠模型,造模成功后低剂量组[50 mg/(kg.d)]及高剂量组[100mg/(kg.d)]分别给予茵陈多糖干预,1周后检测各组大鼠肝脏生化指标[血清谷丙转氨酶(alanine aminotransferase,ALT)、谷草转氨酶(aspartateaminotransferase,AST)、碱性磷酸酶(alkaline phosphatase,ALP)、直接胆红素(direct bilirubin,DBIL)及间接胆红素(indirect bilirubin,IBLI)]及氧化还原酶[超氧化物歧化酶(erythrocuprein,SOD)、丙二醛(malonaldehyde,MDA)、谷胱甘肽过氧化物酶(glutathione peroxidase,GPx)、过氧化氢酶(catalase,CAT)]活力变化。结果茵陈多糖干预1周后,低剂量组及高剂量组血清ALT、AST、ALP、DBIL及IBLI水平明显低于模型组(P<0.05),低剂量组及高剂量组间差异有统计学意义(P<0.05)。低剂量组及高剂量组肝组织匀浆MDA水平低于模型组(P<0.05),SOD、GPx,、CAT平高于模型组(P<0.05),低剂量组同高剂量组间差异有统计学意义(P<0.05)。结论茵陈多糖能够减轻妊娠胆汁淤积大鼠肝脏氧化损伤,发挥对肝功能的保护作用。

Objective To investigate the protective effects of capillary artemisia polysaccharide on liver oxidative damage rats with intrahepatic cholestasis of pregnancy （ICP）. Methods 32 SD rats were divided into the control group （CG）, model group （MG）, high-dose group （HG） and low-dose group （LG） with random digits table. Animal model of ICP were made with injecting estradiol benzoate in rats with 16 weeks of pregnancy except CG. Rats in HG [100 mg/ （kg.d）] and LG [（50 mg/（kg .d）） were interfered with artemisia capillaries polysaccharides. Biochemical indicators in rats liver （serum ALT, AST, ALP, DBIL and IBLI） and oxidordeuctase （level of SOD, MDA, GPx and CAT） were detected after 1 week＇s intervention. Results After 1 week＇s intervention by artemisia capillaries polysaccharides, levels of ALT, AST, ALP, DBIL and IBLI in HG and LG were lower than those in MG （P 〈 0.05）, which also had significant differences between LG and HG （P 〈 0.05）. Levels of MDA in HG and LG were lower than those in MG （P 〈 0.05）, but levels of SOD, GPx and CAT in HG and LG were higher than those in MG （P 〈 0.05）, which also had significant differences between LG and HG （P 〈 0.05）. Conclusion Artemisia capillaries polysaccharides can decrease liver oxidative damage of rats with ICP, and has protective effect for liver function.