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

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 C...

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Bibliographic Details
Published in:Inflammation 2017-04, Vol.40 (2), p.523-529
Main Authors: Ye, Han-Yang, Jin, Jian, Jin, Ling-Wei, Chen, Yan, Zhou, Zhi-Hong, Li, Zhan-Yuan
Format: Article
Language:English
Subjects:
Acute Kidney Injury - drug therapy
Acute Kidney Injury - prevention & control
Animals
Biomedical and Life Sciences
Biomedicine
Chlorogenic Acid - pharmacology
Chlorogenic Acid - therapeutic use
Cytokines - metabolism
Dose-Response Relationship, Drug
Immunology
Inflammation Mediators - metabolism
Internal Medicine
Lipopolysaccharides
Mice
NF-kappa B - metabolism
Original Article
Pathology
Pharmacology/Toxicology
Rheumatology
Signal Transduction - drug effects
Toll-Like Receptor 4 - metabolism
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Summary: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.
ISSN:0360-3997
1573-2576
DOI:10.1007/s10753-016-0498-9