波多辛
达帕格列嗪
医学
自噬
尼福林
糖尿病
肾
糖尿病肾病
内科学
足细胞
内分泌学
纤维化
氧化应激
HMGB1
内质网
肾脏疾病
泌尿科
2型糖尿病
细胞凋亡
蛋白尿
炎症
生物
细胞生物学
生物化学
作者
Bin Feng,Fan Yang,Jie Liu,Qi-Chao Sun,Ran Meng,Dalong Zhu
标识
DOI:10.1016/j.jdiacomp.2023.108409
摘要
Diabetic kidney disease (DKD) is a major cause of chronic and end-stage renal disease in diabetic patients. Here, we investigated protective effects and possible mechanisms of dapagliflozin on renal injury in diabetic mice. DKD mice were established by high fat diet (HFD) feeding. Half of DKD mice were randomly assigned to receive dapagliflozin treatment (200 μg/day) for 8 weeks. Renal lipid droplets, fibrosis, oxidative and endoplasmic reticulum stress were evaluated. Glomerular injury was assessed by immunohistochemistry and transmission electron microscopy. Dapagliflozin led to marked inhibition of ROS levels and endoplasmic reticulum stress in diabetic mice. HFD-induced loss of Podocin and Nephrin, and impaired podocytes were also improved with the treatment. Importantly, overexpression of HMGB1 and suppressed autophagy in the kidney were partly reversed by dapagliflozin. Therefore, we speculate that protective effects of dapagliflozin on DKD may be associated with suppression of HMGB1 expression and restoration of autophagy in the kidney.
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