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

• GEI has a hepatoprotective effect on CCl4-induced hepatic injury and fibrosis.
• GEI effectively suppresses inflammatory response.
• GEI markedly inhibits NF-κB activation.
• GEI significantly suppresses TGF-β1/Smad signaling pathway.

The hepatoprotective effect of Gypsophila elegans isoorientin (GEI) 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-α, IL-1β and IL-6 via inhibiting nuclear factor-κB (NF-κB) activation. In addition, GEI down-regulated the phosphorylation of Smad2/3 and up-regulated the level of hepatic Smad7, thereby inhibiting TGFβ1/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-κB and TGF-β1/Smad signaling pathways.