荞麦黄酮对1型糖尿病小鼠肾损伤的保护作用

Protective effects of buckwheat flavones on kidney injury in type 1 diabetes mice

目的：观察荞麦黄酮对1型糖尿病小鼠肾损伤的保护作用及其机制。方法：小鼠腹腔注射四氧嘧啶100mg/kg,每隔7d注射一次,连续3次,建立小鼠1型糖尿病肾病模型。将成模小鼠随机分为模型对照组、荞麦黄酮低、中、高剂量组（50、100、200mg/kg）及厄贝沙坦组（25mg/kg）,另设正常组。造模后各组小鼠灌胃给药1次/d,连续4w。给药前及给药期间每隔1w用血糖仪测定小鼠空腹血糖（FBG）,末次给药后肾称重,计算肾指数,采用全自动生化仪测定血清中血肌酐、尿素氮,采用ELISA测定尿微量白蛋白含量。肾组织匀浆测定糖基化终产物（AGEs）,超氧化物歧化酶（SOD）及丙二醛（MDA）含量。HE染色观察各组小鼠肾组织形态。结果：与正常组比较,模型对照组小鼠空腹血糖连续4 w持续升高、血肌酐、血尿素氮、尿微量白蛋白、肾指数、肾组织中AGEs、MDA均明显增高,而SOD水平下降,且肾组织形态明显损伤。与模型对照组比较,荞麦黄酮在50~200mg/kg剂量范围均可改善上述指标,在100mg/kg剂量下作用更为明显。结论：荞麦黄酮对1型糖尿病小鼠肾损伤具有一定保护作用,其机制与降低体内AGEs、MDA水平,增加SOD水平相关。

Objective： To investigate protective effect and mechanism of buckwheat flavones on kidney injury in type 1 diabetes mice and explore its mechanisms. Methods： The model of kidney injury in type 1 diabetes mice was made by intraperitoneal injecting alloxan（ once per week,for3 times）. The model mice were randomly divided into model control group,buckwheat flavones groups with various dosages（ 50,100 and 200 mg / kg） and nimodipine group（ 25 mg / kg）,except for normal group. The mice were given drugs by ig administration once per day,for 4 w.The fasting blood glucose（ FBG） was determined every week by glucometer. The kidney index,creatinine,urea nitrogen in serum,and Advanced Glycation End Products（ AGEs） superoxide dismutase（ SOD）,Methane Dicarboxylic Aldehyde（ MDA） in kidney tissues were tested after administration. Results： Compared with normal group,FBG increased continuously in 4 w,the kidney index,the levels of creatinine,urea nitrogen in serum and AGEs,MDA in kidney tissues were all decreased,while SOD level increased（ P 〈 0. 05,P 〈 0. 01）,and kidney tissues were injured remarkablely in model group. Compared with model group,the buckwheat flavones at the dose of 50 ~ 200 mg / kg could improve above each index,and it had the most significant role at the dose of 100 mg / kg（ P 〈 0. 05,P 〈 0. 01）. Conclusion： The buckwheat flavones had protective effects on injury kidney injury in type 1 diabetes mice,its mechanisms are in part associated with decreasing the levels of AGEs,MDA and increasing the level of SOD.