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Research Article

Chikusetsusaponin V attenuates lipopolysaccharide-induced liver injury in mice

, , , , , , , , & show all
Pages 167-174 | Received 28 May 2015, Accepted 01 Feb 2016, Published online: 16 Mar 2016
 

Abstract

Chikusetsusaponin V (CsV), a saponin from Panax japonicus, has been reported to inhibit inflammatory responses in lipopolysaccharide (LPS)-induced macrophage cells. However, whether CsV could alleviate LPS-induced liver injury in vivo and the potential mechanisms involved remain unclear. In the present study, we investigated the anti-inflammatory effects of CsV on LPS-induced acute liver injury in mice and further explored the potential mechanisms involved. Our results showed that CsV significantly attenuated elevation of alanine transaminase (ALT) and aspartate aminotransferase (AST) levels and improved liver histopathological changes in LPS-induced mice. In addition, CsV decreased serum tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) levels and inhibited mRNA expressions of inducible nitric oxide synthase (iNOS), TNF-α and IL-1β in LPS challenged mice. Furthermore, CsV inhibited nuclear factor kappa B (NF-κB) activation by downregulating phosphorylated NF-κB, IκB-α, ERK, c-Jun N-terminal kinase (JNK) and p38 levels in the liver tissue, which ultimately decreased nucleus NF-κB protein level. In conclusion, our data suggested that CsV could be a promising drug for preventing LPS challenged liver injury since it attenuated LPS-induced inflammatory responses, partly via inhibiting NF-κB and MAPK signaling pathways.

Disclosure statement

The authors declare that there are no conflicts of interest.

This work was supported by the grants from the National Nature and Science Foundation of China (NSFC) (No. 81374001) to Ting Wang, the NSFC (No. 81273895) and the Foundation for Innovative Research Groups of the Hubei Province Natural Science Foundation of China (No. 2013CFA014) to Yuan Ding, the Talent Science Foundation of China Three Gorges University (No. KJ2013B0555) to Zhou Zhiyong.

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