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.
Highlights
Acute kidney injury (AKI), as a serious disease, suffered about one in five patients in emergency cases [1]
The levels of blood urea nitrogen (BUN) and creatinine induced by LPS were dose-dependently inhibited by hyperin (25, 50, 100 mg/kg)
We evaluated the protective effects of hyperin on LPS-induced acute kidney injury in mice
Summary
Acute kidney injury (AKI), as a serious disease, suffered about one in five patients in emergency cases [1]. AKI becomes a common and dangerous factor for death progressively [2, 3]. LPS, the outer membrane component of gram-negative bacteria, has been identified as the major factor that leads to AKI [6]. In the mice model of LPSinduced AKI, LPS significantly induces the release of inflammatory cytokines which promote kidney disease [7]. Studies showed that inflammatory cytokines TNF-α, IL6,and IL-1β played critical roles in the pathologicprocess of kidney injury [8]. Inhibition of these inflammatory cytokines could attenuate the injury of kidney tissues.
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