Chlorogenic Acid Attenuates Lipopolysaccharide-Induced Acute Kidney Injury by Inhibiting TLR4/NF-κB Signal Pathway

• DOI: 10.1007/s10753-016-0498-9
• Publication Date: 2016-12-27T03:23:37Z
• Authors: Han-Yang Ye; Jian Jin; Ling-Wei Jin; Yan Chen; Zhi-Hong Zhou; Zhan-Yuan Li
• Keywords: Lipopolysaccharides; 0301 basic medicine; 0303 health sciences; Dose-Response Relationship, Drug; NF-kappa B; Acute Kidney Injury; 3. Good health; Toll-Like Receptor 4; Mice; 03 medical and health sciences; Animals; Cytokines; Chlorogenic Acid; Inflammation Mediators; Signal Transduction

Chlorogenic acid (CGA), a polyphenolic compound, exists widely in medicinal herbs, which has been shown a strong antioxidant and anti-inflammatory effect. This study investigated the protective effects and mechanism of CGA on lipopolysaccharide (LPS)-induced acute kidney injury (AKI). Treatment of CGA successfully ameliorates LPS-induced renal function and pathological damage. Moreover, CGA dose-dependently suppressed LPS-induced blood urea nitrogen (BUN), creatinine levels, and inflammatory cytokines TNF-α, IL-6, and IL-1β in serum and tissue. The relative proteins' expression of TLR4/NF-κB signal pathway was assessed by western blot analysis. Our results showed that CGA dose-dependently attenuated LPS-induced kidney histopathologic changes, serum BUN, and creatinine levels. CGA also suppressed LPS-induced TNF-α, IL-6, and IL-1β production both in serum and kidney tissues. Furthermore, our results showed that CGA significantly inhibited the LPS-induced expression of phosphorylated NF-κB p65 and IκB as well as the expression of TLR4 signal. In conclusion, our results provide a mechanistic explanation for the anti-inflammatory effects of CGA in LPS-induced AKI mice through inhibiting TLR4/NF-κB signaling pathway.