Hyperin protects against LPS-induced acute kidney injury by inhibiting TLR4 and NLRP3 signaling pathways

// Gong Chunzhi 1, 2 , Li Zunfeng 2 , Qin Chengwei 2 , Bu Xiangmei 2 , Yu Jingui 1 1 Department of Anesthesiology, Qilu Hospital, Shandong University, Jinan, 250012, China 2 Department of Anesthesiology, Affiliated Hospital of Binzhou Medical University, Binzhou, 256603, China Correspondence to: Yu Jingui, email: yujinguijj@sina.com Keywords: hyperin, LPS, kidney injury, TLR4, NLRP3 Received: September 06, 2016      Accepted: September 23, 2016      Published: November 01, 2016 ABSTRACT 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.