Gypsophila elegans isoorientin attenuates CCl4-induced hepatic fibrosis in rats via modulation of NF-κB and TGF-β1/Smad signaling pathways

被引:60
作者
Lin, Xing [1 ]
Chen, Yongxin [1 ]
Lv, Shujuan [1 ]
Tan, Shimei [1 ]
Zhang, Shijun [1 ]
Huang, Renbin [1 ]
Zhuo, Lang [1 ]
Liang, Shuang [2 ]
Lu, Zhongpeng [2 ]
Huang, Quanfang [2 ]
机构
[1] Guangxi Med Univ, Nanning 530021, Peoples R China
[2] Guangxi Univ Chinese Med, Affiliated Hosp 1, Nanning 530023, Peoples R China
基金
中国国家自然科学基金;
关键词
Gypsophila elegans; Isoorientin; Hepatic fibrosis; NF-kappa B; TGF-beta; 1/Smad; LIVER FIBROSIS; STELLATE CELLS; CARBON-TETRACHLORIDE; OXIDATIVE STRESS; IN-VITRO; FIBROGENESIS; MECHANISMS; PROGRESSION; EXPRESSION; INSIGHTS;
D O I
10.1016/j.intimp.2015.06.021
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
071005 [微生物学]; 100108 [医学免疫学];
摘要
The hepatoprotective effect of Gypsophila elegans isoorientin (GEL) was evaluated using a hepatic fibrosis model induced by CCl4 in rats. The results revealed that GEI significantly prevented CCl4-induced liver injury and fibrosis, as evidenced by the attenuation of histopathological changes, the decrease in serum aminotransferase, and the inhibition of collagen accumulation. GEI strongly inhibited lipid peroxidation and recruited anti-oxidative defense system. Moreover, GEI alleviated pro-inflammatory cytokines such as TNF-alpha, IL-1 beta and IL-6 via inhibiting nuclear factor-kappa B (NF-kappa B) activation. In addition, GEI down-regulated the phosphorylation of Smad2/3 and up-regulated the level of hepatic Smad7, thereby inhibiting TGF beta 1/Smad signaling pathway. In conclusion, our findings indicate that GEI can inhibit CCl4-induced hepatic fibrosis, which may be ascribed to its radical scavenging action, antioxidant activity, and modulation of NF-kappa B and TGF-beta 1/Smad signaling pathways. (C) 2015 Elsevier B.V. All rights reserved.
引用
收藏
页码:305 / 312
页数:8
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