黄芪对脾虚大鼠小肠葡萄糖吸收功能的影响及机制

Effect and Mechanism of Astragali Radix on the Intestinal Absorption of Glucose in Model Rats with Spleen-qi Deficiency Pattern

目的探讨黄芪对脾虚证大鼠模型小肠黏膜葡萄糖吸收功能的影响及其作用机制。方法采用皮下连续注射利血平注射液(0.5 mg·kg^(-1))14 d建立脾虚证大鼠模型。大鼠随机分为正常组、造模组,并将造模成功的大鼠随机分为模型组、黄芪组(6.0 g·kg^(-1)),连续给药21 d。每日记录大鼠体质量;分别于造模结束和给药结束后收集大鼠尿液,采用硫酸苯酚法测定尿D-木糖排泄率;采用大鼠在体空肠灌流实验及葡萄糖氧化酶法测定葡萄糖吸收量;蛋白免疫印迹法(Western Blot)测定钠依赖葡萄糖转运蛋白(SGLT1)和2型葡萄糖转运蛋白(GLUT2)的蛋白表达;荧光定量PCR法测定SGLT1/GLUT2的m RNA表达。结果与正常组比较,造模组大鼠体质量及模型组大鼠尿D-木糖排泄率、葡萄糖吸收量、SGLT1/GLUT2蛋白相对表达量、SGLT1/GLUT2 m RNA相对表达量均明显降低,差异有统计学意义(P<0.01)。与模型组比较,黄芪组大鼠尿D-木糖排泄率、葡萄糖吸收量、SGLT1/GLUT2蛋白相对表达量、SGLT1/GLUT2 m RNA相对表达量均明显提高,差异有统计学意义(P<0.05,P<0.01)。结论黄芪能够改善利血平致脾虚证大鼠小肠对葡萄糖的吸收功能,其机制可能与调节SGLT1/GLUT2的蛋白表达有关。

Objective To observe the effect of Astragali radix on the intestinal absorption of glucose in model rats with syndrome of Spleen-qi deficiency and investigate its relevant regulation mechanism. Methods Model rats were established by subcutaneous injection of reserpine（0.5 mg·kg-1）on the neck for 14 d. The rats were randomly divided into normal group,model group,and therapy of Astragali radix group（6.0 g·kg-1）. The treatment lasted for 21 d and the rats＇ body weight was collected everyday. Urine samples were collected at the end of modeling and treatment,respectively. Urine D-xylose excretion rate was measured by sulfuric acid phenol method. The glucose uptake was measured by jejunum perfusion and glucose oxidase method. The intestinal mucosa was collected to detect the protein and m RNA expression levels of sodium-dependent glucose transporter 1（SGLT1） and glucose transporter 2（GLUT2）by Western Blot and quantitative PCR methods. Results Compared with the normal group, the body weight,D-xylose excretion rates,glucose uptake,protein and m RNA expression levels of SGLT1 and GLUT2 decreased in the model group（P 〈0.01）. Compared with the model group,the target parameters have been significantly improved by the treatment of Astragali radix（P〈0.05,P〈0.01）. Conclusion Astragali radix can improve the intestinal glucose absorption function of model rats with syndrome of Spleen-qi deficiency; its mechanism may be relevant to the regulation of SGLT1/GLUT2.