荞麦黄酮对大鼠糖尿病肾病的保护作用

目的:观察荞麦黄酮对大鼠糖尿病肾病的保护作用及其机制。方法:SD大鼠ip四氧嘧啶150 mg·kg-1,每隔7 d注射一次,连续3次,建立大鼠糖尿病肾病模型。将成模大鼠随机分为模型组、荞麦黄酮低、中、高剂量组(50,100,200 mg·kg-1)及厄贝沙坦组(17 mg·kg-1),另设正常组。造模后各组大鼠ig给药1次/d,连续12周。给药前及给药后每隔3周测定大鼠空腹血糖(FBG)及24 h尿蛋白含量,末次给药后2 h处死大鼠,采用生化仪测定血清中血肌酐(SCr),尿素氮(BUN),甘油三酯(TG),总胆固醇(TC)水平。肾组织匀浆测定果糖胺(FTS),糖基化终产物(AGEs),超氧化物歧化酶(SOD)及丙二醛(MDA)水平。透射电镜观察各组大鼠肾组织形态。结果:与正常组比较,模型组大鼠FBG和24 h尿蛋白含量持续升高,血清中SCr,BUN,TG,TC水平及肾组织中FTS,AGEs,MDA含量均明显增高,SOD水平下降(P0.05,P0.01),且肾组织形态明显损伤。与模型组比较,荞麦黄酮各剂量组可不同程度改善上述指标,且中剂量组作用更为明显(P0.05,P0.01)。结论:荞麦黄酮对糖尿病肾病大鼠具有一定保护作用,其机制与其具有降糖、降脂、降低非酶糖基化及氧化应激水平相关。

Protective Effects of Buckwheat Flavones on Diabetic Nephropathy Rats

Objective: To investigate the protective effect and mechanism of buckwheat flavones on diabetic nephropathy rats. Method: The model of diabetic nephropathy rats was made by intraperitoneally injecting alloxan once per week for 3 times. The rats were randomly divided into the model control group, the buckwheat flavones groups (50, 100, 200 mg · kg^-1), the irbesartan group (25 mg · kg^-1) and the normal group. The rats were intragastrically administrated of the corresponding medicines once daily for 12 weeks. The fasting blood glucose (FBG) and 24-h urine protein were determined every 3 weeks. The levels of serum creatinine (SCr), blood urea nitrogen (BUN), triglyceride (TG), total cholesterol (TC) in serum were tested by auto analyzer, and the levels of fructosamine (FTS), advanced glycation end products (AGEs), superoxide dismutase (SOD), and methane dicarboxylic aldehyde (MDA) in kidney tissues were tested after the treatment. Result: Compared with the normal group, FBG and 24-h urine protein increased continuously, the levels of SCr, BUN, TG, TC in serum and FTS, AGEs, MDA in kidney tissues decreased, the SOD level increased (P<0.05,P<0.01), and kidney tissues were injured remarkably in model control group. Compared with the model control group, the buckwheat flavones could improve the above indexes (P<0.05, P<0.01). Conclusion: The buckwheat flavones have protective effects on diabetic nephropathy rats, and its mechanisms are in part associated with reducing blood glucose, blood lipid, and decreasing non-enzymatic glycosylation and oxidative stress.