Hyperin protects against LPS-induced acute kidney injury by inhibiting TLR4 and NLRP3 signaling pathways
Metrics: PDF 2566 views | HTML 3083 views | ?
Gong Chunzhi1,2, Li Zunfeng2, Qin Chengwei2, Bu Xiangmei2, Yu Jingui1
1Department of Anesthesiology, Qilu Hospital, Shandong University, Jinan, 250012, China
2Department of Anesthesiology, Affiliated Hospital of Binzhou Medical University, Binzhou, 256603, China
Yu Jingui, email: [email protected]
Keywords: hyperin, LPS, kidney injury, TLR4, NLRP3
Received: September 06, 2016 Accepted: September 23, 2016 Published: November 01, 2016
Hyperin is a flavonoid compound derived from Ericaceae, Guttifera, and Celastraceae that has been shown to have various biological effects, such as anti-inflammatory and anti-oxidant effects. However, there is no evidence to show the protective effects of hyperin on lipopolysaccharide (LPS)-induced acute kidney injury (AKI). Therefore, we investigated the protective effects and mechanism of hyperin on LPS-induced AKI in mice. The levels of TNF-α, IL-6, and IL-1β were tested by ELISA. The effects of hyperin on blood urea nitrogen (BUN) and serum creatinine were also detected. In addition, the expression of TLR4, NF-κB, and NLRP3 were detected by western blot analysis. The results showed that hyperin significantly inhibited LPS-induced TNF-α, IL-6, and IL-1β production. The levels of BUN and creatinine were also suppressed by hyperin. Furthermore, LPS-induced TLR4 expression and NF-κB activation were also inhibited by hyperin. In addition, treatment of hyperin dose-dependently inhibited LPS-induced NLRP3 signaling pathway. In conclusion, the results showed that hyperin inhibited LPS-induced inflammatory response by inhibiting TLR4 and NLRP3 signaling pathways. Hyperin has potential application prospects in the treatment of sepsis-induced AKI.
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.