红芪多糖减缓糖尿病肾病小鼠病程进展的作用机制研究

Study on the effective mechanisms of Hedysarum polybotrys polysacchcaide on delay the development of diabetic nephropathy in mice with diabetic nephropathy

目的探讨红芪多糖(HPS)对糖尿病肾病db/db小鼠肾的保护机制。方法将50只5周龄的雄性db/db小鼠随机分为5组:高中低3个剂量实验组,替米沙坦对照组,模型组,正常组(10只同周龄的db/m小鼠)。于6周龄时,灌胃给药,连续8周,分别给予200,100,50 mg·kg-1HPS、替米沙坦5 mg·kg-1和等体积0.9%Na Cl。第8周末,收集小鼠24 h尿,检测24 h尿蛋白排泄量后,处死小鼠,眼球取血,分离血清并测定相关指标。结果给药8周后,血肌酐(Scr)和24 h蛋白尿排泄量均较模型组明显降低(P<0.05,P<0.01);血糖、血尿素氮(BUN)、p38丝裂原活化蛋白激酶(P38MAPK)蛋白表达、P38MAPK mRNA表达及基质金属蛋白酶(MMPs)mRNA表达与模型组比较,只有高、中2个剂量HPS组差异有统计学意义(P<0.05)。结论红芪多糖可能通过抑制db/db小鼠肾小球系膜细胞上P38MAPK和MMPs蛋白及mRNA的表达,从而减缓糖尿病肾病的病程进展。

Objective To investigate the protection effect of Hedysarum polybotrys polysacchcaide （ HPS） on early diabetic nephropathy （ DN） in db/db mice.Methods Fifty db/db male mice （ five weeks old ） were randomly divided into five groups：HPS （ low-dose , mid-dose , hing-dose） groups, telmisartan group, model group.Ten db/m mice （ five weeks old ） were employed as normal group.At the beginning of 6 weeks, were respectively given 200,100, and 50 mg · kg -1 HPS; 5 mg· kg-1 telmisartan.The mice in normol group and model group were given 0.9%NaCl by gavege.The 24 hours urine protein were measured after administration 8 weeks and kill the mice with remove blood and serum was isolated from the eye .And the related indexes were evaluated.Results After interventing 8 weeks,compared with model group , serum creatinine （ Scr） 24 hours urine proteinall in HPS and telmisartan groups decreased （ P〈0.05 ）.The levels of blood glucose , blood urea nitrogen （ BUN ） , the expression of p 38 mitogen -activated protein kinase （ p38 MAPK ） and matrix metalloproteinases （ MMPs ） mRNA all decreased , but only the high , middle doses groups of HPS were statisti-cally difference （ P 〈0.05 ） .Conclusion Which indicates that HPS＆nbsp;could delay the development of DN by inhibiting the P 38MAPK,MMPs protein and mRNA expression in the glomerular mesangial cell membrane.