Abstract |
Tenuigenin (TNG) has been reported to have various pharmacological activities, such as anti-oxidative and anti-inflammatory activities. However, the protective effects of TNG on lipopolysaccharides (LPS)-induced acute kidney injury (AKI) are still not clear. The aim of this study was to investigate the protective effects and mechanism of TGN on LPS-induced AKI in mice. The kidney histological change, levels of blood urea nitrogen (BUN), and creatinine were measured to assess the protective effects of TNG on LPS-induced AKI. The levels of TNF-α, IL-1β, and IL-6 in serum and kidney tissues were detected by ELISA. The extent of nuclear factor kappa-B (NF-κB) p65 and the expression of Toll-like receptor-4 (TLR4) were detected by western blot analysis. The results showed that TNG markedly attenuated the histological alterations, BUN and creatinine levels in kidney. TNG also suppressed LPS-induced TNF-α, IL-1β, and IL-6 production. Furthermore, the expression of TLR4 and NF-κB activation induced by LPS were markedly inhibited by TNG. In conclusion, this study demonstrated that TNG protected against LPS-induced AKI by inhibiting TLR4/NF-κB signaling pathway.
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Authors | Haiyan Fu, Zhansheng Hu, Xingwei Di, Qiuhong Zhang, Rongbin Zhou, Hongyang Du |
Journal | European journal of pharmacology
(Eur J Pharmacol)
Vol. 791
Pg. 229-234
(11 15 2016)
ISSN: 1879-0712 [Electronic] Netherlands |
PMID | 27546562
(Publication Type: Journal Article)
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Copyright | Copyright © 2016 Elsevier B.V. All rights reserved. |
Chemical References |
- Cytokines
- Drugs, Chinese Herbal
- Lipopolysaccharides
- Toll-Like Receptor 4
- Transcription Factor RelA
- tenuigenin
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Topics |
- Acute Kidney Injury
(chemically induced, drug therapy, pathology, physiopathology)
- Animals
- Cytokines
(biosynthesis)
- Cytoprotection
(drug effects)
- Drugs, Chinese Herbal
(pharmacology)
- Gene Expression Regulation
(drug effects)
- Kidney
(drug effects, metabolism, pathology, physiopathology)
- Lipopolysaccharides
(adverse effects)
- Male
- Mice
- Mice, Inbred BALB C
- Signal Transduction
(drug effects)
- Toll-Like Receptor 4
(metabolism)
- Transcription Factor RelA
(metabolism)
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