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

Abstract

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.

• Authors: Han-Yang Ye, Jian Jin, Ling-Wei Jin, Yan Chen, Zhi-Hong Zhou, Zhan-Yuan Li
• Journal: Inflammation (Inflammation) Vol. 40 Issue 2 Pg. 523-529 (Apr 2017) ISSN: 1573-2576 [Electronic] United States
• PMID: 28028753 (Publication Type: Journal Article)

Chemical References

• Cytokines
• Inflammation Mediators
• Lipopolysaccharides
• NF-kappa B
• Toll-Like Receptor 4
• Chlorogenic Acid

Topics

• Acute Kidney Injury (drug therapy, prevention & control)
• Animals
• Chlorogenic Acid (pharmacology, therapeutic use)
• Cytokines (metabolism)
• Dose-Response Relationship, Drug
• Inflammation Mediators (metabolism)
• Lipopolysaccharides
• Mice
• NF-kappa B (metabolism)
• Signal Transduction (drug effects)
• Toll-Like Receptor 4 (metabolism)