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木犀草素A对脂多糖和/或D-氨基半乳糖诱导的小鼠急性肝损伤的保护作用。

Protective effect of oroxylin A against lipopolysaccharide and/or D-galactosamine-induced acute liver injury in mice.

作者信息

Huang Haiying, Zhang Xiaoyu, Li Jingyuan

机构信息

Department of Infectious Diseases, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.

Department of Infectious Diseases, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.

出版信息

J Surg Res. 2015 May 15;195(2):522-8. doi: 10.1016/j.jss.2015.01.047. Epub 2015 Jan 30.

Abstract

BACKGROUND

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).

METHODS

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.

RESULTS

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.

CONCLUSIONS

In conclusion, oroxylin A protected against LPS and/or GalN-induced liver injury through activating Nrf2 and inhibiting TLR4 signaling pathway.

摘要

背景

木犀草素A是从黄芩中分离出的一种天然黄酮类化合物,据报道具有广泛的药理活性。然而,木犀草素A对肝损伤的影响尚不清楚。本研究旨在探讨木犀草素A对脂多糖和/或D-半乳糖胺(LPS和/或D-GalN)诱导的小鼠急性肝损伤的影响。

方法

用LPS(50μg/kg)和/或GalN(800mg/kg)诱导小鼠急性肝损伤模型。分析血清丙氨酸氨基转移酶、天冬氨酸氨基转移酶和肿瘤坏死因子-α水平、肝组织组织学、丙二醛含量和髓过氧化物酶活性。同时,通过蛋白质免疫印迹法检测核因子κB(NF-κB)、血红素加氧酶-1(HO-1)和核因子红细胞2相关因子2(Nrf2)的表达。

结果

结果表明,木犀草素A剂量依赖性地抑制LPS和/或GalN诱导的血清丙氨酸氨基转移酶、天冬氨酸氨基转移酶和肿瘤坏死因子-α水平。木犀草素A还抑制了肝脏丙二醛含量和髓过氧化物酶活性。我们还发现木犀草素A抑制LPS和/或GalN诱导的Toll样受体4(TLR4)表达和NF-κB激活。此外,木犀草素A以剂量依赖性方式上调Nrf2和HO-1的表达。

结论

总之,木犀草素A通过激活Nrf2和抑制TLR4信号通路来保护小鼠免受LPS和/或GalN诱导的肝损伤。

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