Chen Zhou-xiong, Xie Xiao-yun, Yu Ri-chen, Zhang Jun, Lei Min-xiang
Department of Endocrinology, Xiangya Hospital, Central South University, Changsha 410008, China.
Zhong Nan Da Xue Xue Bao Yi Xue Ban. 2008 Oct;33(10):906-12.
To investigate the effect of diet-induced hyperlipidemia on TGF-beta/Smad signaling pathway in the kidney of diabetic rats, and to explore the mechanism by which hyperlipidemia leads to renal injury in diabetes.
Diabetic rats and non-diabetic rats were fed with normal fat diet and high fat diet for 16 weeks, respectively. The expressions of TGF-beta1, TbetaRII, and Col-IV mRNA in the renal cortex were examined by reverse transcriptase-PCR,TbetaRII and p-Smad staining in glomerular cells were detected by immunohistochemical staining, and the expression of TGF-beta1 and Col-IV protein was determined by Western blot.
Diet-induced hyperlipidemia up-regulated the levels of TGF-beta1, TbetaRII, p-Smad, and Col-IV protein and mRNA in the renal cortex of diabetic rats compared with those of non-diabetic rats. However, feeding high fat diet to non-diabetic rats had no influence on the expression of TGF-beta1, TbetaRII, p-Smad2, and Col-IV in the renal cortex.
Hyperlipidemia induced by high fat diet ingestion leads to renal injury in diabetic rats through activating TGF-beta1 /Smad signaling pathway.
探讨饮食诱导的高脂血症对糖尿病大鼠肾脏中转化生长因子-β(TGF-β)/Smad信号通路的影响,并探究高脂血症导致糖尿病肾损伤的机制。
将糖尿病大鼠和非糖尿病大鼠分别给予正常脂肪饮食和高脂饮食喂养16周。采用逆转录聚合酶链反应(RT-PCR)检测肾皮质中TGF-β1、TβRII和IV型胶原(Col-IV)mRNA的表达;采用免疫组织化学染色检测肾小球细胞中TβRII和磷酸化Smad(p-Smad)的染色情况;采用蛋白质免疫印迹法检测TGF-β1和Col-IV蛋白的表达。
与非糖尿病大鼠相比,饮食诱导的高脂血症上调了糖尿病大鼠肾皮质中TGF-β1、TβRII、p-Smad和Col-IV蛋白及mRNA的水平。然而,给予非糖尿病大鼠高脂饮食对其肾皮质中TGF-β1、TβRII、p-Smad2和Col-IV的表达无影响。
高脂饮食摄入诱导的高脂血症通过激活TGF-β1/Smad信号通路导致糖尿病大鼠肾损伤。