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目的观察饮食中晚期糖基化终产物(AGEs)对糖尿病肾病(DN)大鼠肾脏的影响,探讨其作用机制。方法 SD大鼠40只,随机选取10只为空白对照组,30只大鼠DN模型建立成功,随机分为3组:高AGEs饲料组、低AGEs饲料组及普通饲料组,每组10只。分别于第9周及第13周对各组大鼠进行检测:考马斯亮蓝法测定24h尿蛋白量,速率法测定血肌酐(Scr)和尿肌酐,硫代巴比妥酸反应法(TBARS)测定24h尿及肾组织匀浆中丙二醛(MDA)含量,ELISA法测定血清及肾组织匀浆中羧甲基赖氨酸(CML)含量,比色法测定血清及肾组织匀浆中硒谷胱甘肽过氧化物酶(SeGSHPx)活性,计算内生肌酐清除率(Ccr)。结果 3组DN大鼠各指标与空白对照组相比,差异有统计学意义(P<0.05)。与普通饲料组相比,高AGEs饲料组大鼠24h尿蛋白、24h尿及肾组织匀浆中MDA含量、血清及肾组织匀浆中CML含量显著增加(P<0.05),血清及肾组织匀浆中SeGSHPx活性显著降低(P<0.05);低AGEs饲料组大鼠24h尿蛋白、24h尿及肾组织匀浆中MDA含量、血清及肾组织匀浆中CML含量显著减少(P<0.05),血清及肾组织匀浆中SeGSHPx活性显著升高(P<0.05)。3组DN大鼠之间Scr及Ccr差异无统计学意义(P>0.05)。结论高AGEs饲料促进DN大鼠肾功能恶化,其作用机制与抗氧化体系受损、氧化应激增强有关。
Objective To investigate the effects of dietary advanced glycosylation end products (AGEs) on the kidneys of diabetic nephropathy rats and to explore its mechanism. METHODS: Forty Sprague-Dawley rats were randomly divided into control group and control group. Ten rats were randomly divided into three groups: high AGEs diet group, low AGEs diet group and normal feed group, with 10 rats in each group. At the 9th week and the 13th week respectively, the rats in each group were tested: Coomassie brilliant blue method was used to determine the amount of urinary protein in 24 hours, the serum creatinine (Scr) and creatinine were measured by the rate method, the thiobarbituric acid reaction method (TBARS) The content of malondialdehyde (MDA) in 24h urine and renal homogenate was measured. The contents of carboxymethyl lysine (CML) in serum and kidney homogenate were measured by ELISA. The content of selenium in serum and kidney homogenate Glutathione peroxidase (SeGSHPx) activity, calculated creatinine clearance (Ccr). Results The indexes of DN rats in 3 groups were significantly different from those in control group (P <0.05). Compared with the normal feed group, the 24 h urinary protein, 24h urine and renal tissue homogenate MDA content, serum and renal homogenate CML content increased significantly (P <0.05), serum and kidney homogenate (P <0.05). The content of MDA in 24 h urinary protein, 24 h urine and kidney homogenate, and the content of CML in serum and kidney homogenate decreased significantly in low AGEs diet group (P <0.05) Serum and renal tissue homogenate SeGSHPx activity was significantly increased (P <0.05). There was no significant difference in Scr and Ccr between the three groups of DN rats (P> 0.05). Conclusions High AGEs diet can promote the deterioration of renal function in DN rats. The mechanism of action is related to the impaired antioxidant system and the increased oxidative stress.