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首页> 外文期刊>International immunopharmacology >Gypsophila elegans isoorientin attenuates CCl4-induced hepatic fibrosis in rats via modulation of NF-kappa B and TGF-beta 1/Smad signaling pathways
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Gypsophila elegans isoorientin attenuates CCl4-induced hepatic fibrosis in rats via modulation of NF-kappa B and TGF-beta 1/Smad signaling pathways

机译：满天星满天星异味素通过调节NF-κB和TGF-beta 1 / Smad信号通路减弱CCl4诱导的大鼠肝纤维化

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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.
机译：使用CCl4诱导的大鼠肝纤维化模型评估了满天星满天星（orthos elegans isoorientin，GEL）的保肝作用。结果表明，GEI显着预防了CCl4诱导的肝损伤和纤维化，如组织病理学变化的减弱，血清氨基转移酶的降低和胶原蛋白积聚的抑制所证明。 GEI强烈抑制脂质过氧化并募集抗氧化防御系统。此外，GEI通过抑制核因子-κB（NF-κB）活化减轻了促炎性细胞因子，如TNF-α，IL-1β和IL-6。此外，GEI下调Smad2 / 3的磷酸化并上调肝Smad7的水平，从而抑制TGFβ1/ Smad信号通路。总之，我们的发现表明，GEI可以抑制CCl4诱导的肝纤维化，这可能归因于其自由基清除作用，抗氧化活性以及对NF-κB和TGF-β1/ Smad信号通路的调节。 （C）2015 Elsevier B.V.保留所有权利。

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