丙二醛
髓过氧化物酶
肝损伤
药理学
TLR4型
脂多糖
肿瘤坏死因子α
化学
NF-κB
半乳糖胺
医学
受体
生物化学
炎症
氧化应激
内科学
信号转导
氨基葡萄糖
作者
Haiying Huang,Xiaoyu Zhang,Jingyuan Li
标识
DOI:10.1016/j.jss.2015.01.047
摘要
Oroxylin A, a natural flavonoid isolated from Scutellariae baicalensis, has been reported to possess a wide spectrum of pharmacologic activities. However, the effects of oroxylin A on liver injury are poor understood. The purpose of this study was to investigate the effects of oroxylin A on acute liver injury in mice induced by lipopolysaccharide and/or D-galactosamine (LPS and/or D-GalN).Mice acute liver injury model was induced by LPS (50 μg/kg) and/or GalN (800 mg/kg). Serum alanine aminotransferase, aspartate aminotransferase, and tumor necrosis factor-α levels, hepatic tissue histology, malondialdehyde content, and myeloperoxidase activity were analyzed. Meanwhile, nuclear factor kappa B (NF-κB), heme oxygenase-1 (HO-1), and nuclear factor erythroid2-related factor 2 (Nrf2) expression were detected by Western blotting.The results showed that oroxylin A dose-dependently inhibited LPS and/or GalN-induced serum alanine aminotransferase, aspartate aminotransferase, and tumor necrosis factor-α levels. Hepatic malondialdehyde content and myeloperoxidase activity were also suppressed by oroxylin A. We also found that oroxylin A inhibited LPS and/or GalN-induced toll like receptor 4 (TLR4) expression and NF-κB activation. In addition, oroxylin A upregulated the expression of Nrf2 and HO-1 in a dose-dependent manner.In conclusion, oroxylin A protected against LPS and/or GalN-induced liver injury through activating Nrf2 and inhibiting TLR4 signaling pathway.
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