肾
下调和上调
活性氧
炎症
化学
基因敲除
药理学
癌症研究
细胞凋亡
内分泌学
内科学
医学
生物化学
基因
作者
Gui‐Hong Zheng,Qun Shan,Jingjing Mu,Yong‐Jian Wang,Zi-Feng Zhang,Shao‐Hua Fan,Bin Hu,Meng‐Qiu Li,Jun Xie,Ping Chen,Dongmei Wu,Jun Lü,Yuan‐Lin Zheng
摘要
Our preliminary data showed that VEGFR2 upregulation promoted renal ROS overproduction in high-fat diet- (HFD-) treated mice. Given that ROS-induced NLRP3 activation plays a central role in the pathogenesis of type 2 diabetic kidney injury, we evaluate whether VEGFR2 upregulation induces type 2 diabetic kidney injury via ROS-mediated NLRP3 activation and further explore the underlying mechanism. Our results showed that VEGFR2 knockdown decreased ROS overproduction, blocked NLRP3-dependent inflammation, and alleviated kidney damage in HFD-treated mice. Treatment with α-lipoic acid, a scavenger of ROS, lowered ROS overproduction and alleviated NLRP3-triggered kidney injury of HFD-treated mice. Collectively, the VEGFR2/ROS/NLRP3 signal is a critical therapeutic strategy for the kidney injury of HFD-treated mice. Purple sweet potato color (PSPC), a natural anthocyanin, can exert renal protection by inhibiting ROS in HFD-treated mice. Here, we provide a novel mechanism of PSPC against renal damage in HFD-treated mice by downregulating VEGFR2 expression.
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