Purple Sweet Potato Color Attenuates Kidney Damage by Blocking VEGFR2/ROS/NLRP3 Signaling in High-Fat Diet-Treated Mice.
Gui-Hong ZhengQun ShanJing-Jing MuYong-Jian WangZi-Feng ZhangShao-Hua FanBin HuMeng-Qiu LiJun XiePing ChenDong-Mei WuJun LuYuan-Lin ZhengPublished in: Oxidative medicine and cellular longevity (2019)
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.
Keyphrases
- high fat diet
- insulin resistance
- high fat diet induced
- cell death
- dna damage
- adipose tissue
- reactive oxygen species
- oxidative stress
- type diabetes
- poor prognosis
- signaling pathway
- metabolic syndrome
- machine learning
- cell proliferation
- newly diagnosed
- wild type
- smoking cessation
- diabetic rats
- data analysis
- replacement therapy