马斯里酸可预防脂多糖/半乳糖胺诱导的小鼠急性肝损伤。
Maslinic acid protects against lipopolysaccharide/d-galactosamine-induced acute liver injury in mice.
机构信息
Department of Infectious Disease, The Forth Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, China.
Department of Pharmaceutical Preparations, Liaocheng People's Hospital and Liaocheng Clinical School of Taishan Medical University, Liaocheng, Shandong 252000, China.
出版信息
Microb Pathog. 2018 Jun;119:49-53. doi: 10.1016/j.micpath.2018.04.002. Epub 2018 Apr 6.
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.
急性肝损伤是一种危及生命的综合征，通常由肝细胞损伤引起。在这项研究中，我们研究了齐墩果酸（MA）对脂多糖（LPS）/D-半乳糖胺（D-gal）诱导的急性肝损伤的保护作用，并阐明了其机制。通过给予 LPS 和 D-gal 诱导小鼠急性肝损伤模型，在给予 LPS 和 D-gal 前 1 小时通过腹腔内给予 MA。我们的结果表明，MA 通过减轻肝组织病理变化、血清 AST 和 ALT 水平来保护肝脏免受损伤。MA 还抑制了血清和肝组织中炎症细胞因子 TNF-α 和 IL-6 的增加。LPS/D-gal 上调了肝组织中 MDA 的水平和 MPO 的活性，而 MA 呈剂量依赖性抑制了这些变化。此外，MA 减弱了肝 NF-κB 蛋白表达，增加了肝 Nrf2 和 HO-1 蛋白表达。综上所述，MA 通过抑制 NF-κB 和激活 Nrf2 信号通路，对 LPS/D-gal 诱导的肝损伤提供了保护作用。
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