黄芪总苷(AST)对糖尿病小鼠肾脏的保护作用机制

Protective Effect of Total Saponins of Astragalus(AST) on Kidney of Diabetic Mice

探讨黄芪总苷(AST)对糖尿病小鼠肾脏的保护作用及其机制。链脲佐菌素(STZ)诱导制备糖尿病小鼠模型,分为阴性组、阳性组与AST治疗组[给药浓度分别为:30,60,120 mg/(kg·d)],在给药4 w和8 w时,观察各组小鼠的一般情况、体重和血糖浓度,在第8 w观察各组小鼠的肾脏组织病理改变,检测肾小球细胞凋亡指数和肾脏TGF-β1、ColⅣ的mRNA表达。给药8 w后,AST低、中、高浓度组小鼠的体重[(31.32±3.63),(35.59±5.32),(37.21±3.08)g]明显大于阴性组(19.88±2.71)g,血糖水平[(18.47±1.12),(13.15±1.23),(11.79±1.68)mmol/L]明显小于阴性组(21.27±3.15)mmol/L,肾小球PAS阳性分值(23.72±3.57,20.28±3.25,18.36±3.12)明显小于阴性组(42.84±7.23),肾小球细胞凋亡指数[(33.28±5.95)%,(31.21±5.28)%,(24.81±3.49)%]明显小于阴性组(50.35±5.13)%,AST中浓度组小鼠肾脏ColⅣ、TGF-β1的mRNA表达水平(0.51±0.13,0.62±0.11)较阴性组(0.78±0.11,0.82±0.13)均明显下降,上述差异均有统计学意义(P<0.05)。AST可能通过抑制糖尿病小鼠肾脏组织的TGF-β1、ColⅣ的mRNA表达来保护肾脏。

To study the protective effect and mechanism of total saponins of Astragalus （AST） on kidney of diabetic mice,the dia-betic mice model was induced by streptozotocin （STZ） and divided into negative group, positive group and AST high, middle and lowdose groups [ 30,60 and 120 mg/（ kg· d） ]. Within 4 and 8 weeks, the general condition, body weight and blood glucose level of micein each group were observed. At eighth week, the pathological changes of renal tissue were observed in each group and the apoptosisindex of glomenflar cells and the mRNA expression of TGF-β1 and Col 1V were detected. After 8 weeks of treatment,mice weight ofAST low, medium and high dose group [ （31.32 ± 3.63 ）, （35.59 ± 5.32）, （37.21 ± 3.08 ） g ] was significantly greater than that ofthe negative group （ 19.88 ± 2.71 ） g, blood glucose level [ （ 18.47 ±1.12 ）, （ 13. 15 ± 1.23 ）, （ 11.79 ±1.68 ） mmol/L 1 weresignificantly lower than those of negative group （21.27 ±3.15） retool/L, glomerular PAS positive score [ （23.72 ± 3.57 ）, （20.28 ±3.25）, （ 18.36 ± 3.12） ] were significantly less than those of the negative group （42.84 ± 7.23 ）, glomerular cell apoptosis indexes[ （33.28 ±5.95） %, （ 31.21 ± 5.28 ） %, （24.81 ± 3.49 ） % ] were significantly less than these of negative group [ （ 50.35 ±5. 13 ）% ] , the mRNA expression level of Col IV and TGF-β1 in kidney of mice （0. 51 ± 0. 13,0.62 ±O. 11 ） in the middle doseAST group was significantly lower than that of negative group （0.78 ± 0.11,0. 82 ± 0. 13 ）, the differences were statistically signifi-cant （ P 〈 0.05 ）. AST has a protective effect on kidney of STZ diabetic mice and the mechanism may be related to the inhibition ofmRNA expression of Col IV and TGF-β1 in kidney tissue.