College of Chinese Medicinal Materials, Jilin Agricultural University, Changchun, China.
Institute of Translational Medicine, The First Hospital of Jilin University, Changchun, China.
Biomed Pharmacother. 2018 Oct;106:896-901. doi: 10.1016/j.biopha.2018.07.034. Epub 2018 Jul 12.
The purpose of this study was to investigate the hepatoprotective effect of α-mangostin (α-MG) on lipopolysaccharide/d-galactosamine (LPS/D-GalN)-induced acute liver failure and discover its potential mechanisms in mice. The results showed that α-MG could attenuate LPS/D-GalN-induced liver pathological injury, and decrease the hepatic malondialdehyde (MDA) level, serum alanine aminotransferase (ALT), aspartate transaminase (AST), tumor necrosis factor (TNF-α), interleukin-1β and 6 (IL-1β, IL-6) levels and recovery hepatic glutathione (GSH), superoxide dismutase (SOD), catalase (CAT) activities. The results also indicated that α-MG inhibited LPS/D-GalN-induced toll-like receptor 4 (TLR4) expression and NF-κB activation. In addition, α-MG up-regulated the expressions of Nrf2 and heme oxygenase-1 (HO-1). In conclusion, the results indicated that α-MG could protect against LPS/D-GalN-induced liver failure by activating Nrf2 to induce antioxidant defense and inhibiting TLR4 signaling pathway to induce anti-inflammatory effect.
本研究旨在探讨α-倒捻子素（α-MG）对脂多糖/半乳糖胺（LPS/D-GalN）诱导的急性肝衰竭的保护作用，并探讨其在小鼠中的潜在机制。结果表明，α-MG 可减轻 LPS/D-GalN 诱导的肝病理损伤，降低肝丙二醛（MDA）水平、血清丙氨酸氨基转移酶（ALT）、天冬氨酸氨基转移酶（AST）、肿瘤坏死因子（TNF-α）、白细胞介素-1β 和 6（IL-1β、IL-6）水平，并恢复肝谷胱甘肽（GSH）、超氧化物歧化酶（SOD）、过氧化氢酶（CAT）活性。结果还表明，α-MG 抑制了 LPS/D-GalN 诱导的 Toll 样受体 4（TLR4）表达和 NF-κB 激活。此外，α-MG 上调了 Nrf2 和血红素加氧酶-1（HO-1）的表达。综上所述，结果表明，α-MG 通过激活 Nrf2 诱导抗氧化防御，抑制 TLR4 信号通路诱导抗炎作用，从而防止 LPS/D-GalN 诱导的肝衰竭。
