Objective To explore the protection on the kidneys of streptozotocin (STZ)-induced diabetic nephropathy (DN) SD rats, and the related mechanism, by abating miR-200C. Methods The DN SD rat model was constructed through high-glucose and high-fat diet combined with intraperitoneal injection of STZ. Thirty successfully constructed DN model rats were randomly divided into a model group and an observation group, with 15 rats in each group. Additionally, 15 normal healthy SD rats were collected as the control group. After successful modeling, rats in observation group were given a tail vein injection of antagomir-200c (30 mg/kg) every 7 days, while those in model group and control group were given a tail vein injection of equivalent amounts of normal saline. Eight weeks later, the serum creatinine (Cr), blood urea nitrogen (BUN), and 24 h urine protein quantitation (UPQ) level in rats were detected. Meanwhile, miR-200c expression in renal tissues was detected through real-time fluorescence quantitative PCR (qRT-PCR). Histopathological changes in kidneys were observed through HE staining. Reactive oxygen species (ROS) and malondialdehyde (MDA) levels in renal tissues were detected using the ROS and MDA detection kits. In addition, the protein levels of transforming growth factor-β1 (TGF-β1) and fibronectin in renal tissues were also detected through Western blot. Results Compared with the control group, miR-200c expression in renal tissues, serum BUN and Cr levels, 24 h UPQ, renal interstitial injury score, ROS and MDA levels, as well as TGF-β1 and fibronectin protein expression in the model group were all markedly elevated (P＜0.05). Compared with the model group, the above indicators in the observation group were all markedly reduced (P＜0.05). Conclusions miR-200c expression in the renal tissues of STZ-induced DN rats is up-regulated, and abation of miR-200c can partly protect the kidneys of DN rats, which may be related to the reduction of oxidative stress in kidney tissue and the inhibition of TGF-β1 signaling pathway.
Key words
Rat; /
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Diabetic nephropathy; /
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miR-200c; /
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Oxidative stress; /
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TGF-β1
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