Journal
OXIDATIVE MEDICINE AND CELLULAR LONGEVITY
Volume 2019, Issue -, Pages -Publisher
HINDAWI LTD
DOI: 10.1155/2019/5189819
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Funding
- Priority Academic Program Development (PAPD) of the Natural Science Foundation of the Jiangsu Higher Education Institution of China
- 2016 333 Project Award of the Government of Jiangsu Province
- 2013 Qinglan Project of the Young and Middle-aged Academic Leader of Jiangsu College and University
- National Natural Science Foundation of China [81571055, 81400902, 81271225, 31201039, 81171012, 31200873, 81701821, 30950031]
- Major Fundamental Research Program of the Natural Science Foundation of the Jiangsu Higher Education Institution of China [13KJA180001, 16KJB310003]
- Cultivate National Science Fund for Distinguished Young Scholars of Jiangsu Normal University
- Graduate Student Innovation Program of the Government of Jiangsu Province [KYZZ16_0467, KYCX17_1621]
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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 a-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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