| Literature DB >> 29627448 |
Yuan-Yuan Wang1, Bao-Zhong Diao2, Li-Hua Zhong1, Bao-Ling Lu1, Yu Cheng1, Lei Yu3, Li-Ying Zhu4.
Abstract
Acute liver injury is a life-threatening syndrome that often caused by hepatocyte damage. In this study, we investigated the protective effects of maslinic acid (MA) on lipopolysaccharide (LPS)/d-galactosamine (D-gal)-induced acute liver injury and clarified its mechanism. Mice acute liver injury model was induced by given LPS and D-gal and MA was given intraperitoneally 1 h before LPS and D-gal. Our results showed that MA protected against liver injury by attenuating liver histopathologic changes, serum AST and ALT levels. The increased inflammatory cytokines TNF-α and IL-6 in serum and liver tissues were also inhibited by MA. The level of MDA and the activity of MPO in liver tissues were up-regulated by LPS/D-gal and dose-dependently inhibited by MA. Furthermore, MA attenuated hepatic NF-κB protein expression and increased hepatic Nrf2 and HO-1 protein expression. Taken together, MA offers a protective role against LPS/D-gal-induced liver injury through suppressing NF-κB and activating Nrf2 signaling pathways.Entities:
Keywords: Acute liver injury; Lipopolysaccharide; Maslinic acid; NF-κB; d-galactosamine
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Year: 2018 PMID: 29627448 DOI: 10.1016/j.micpath.2018.04.002
Source DB: PubMed Journal: Microb Pathog ISSN: 0882-4010 Impact factor: 3.738