| Hepatic fibrosis is the common wound-healing response, characterized by the excessive deposition of extracellular matrix (ECM) components. During fibrogenic process, transforming growth factor-β1 (TGF-β1) signaling pathway in the activated hepatic stellate cells (HSCs) plays an important role. Naringenin has shown a significantly protective effect on experimental rat liver fibrosis. However, its mechanism has remained unclear. In this study, the inhibitory effects of naringenin on ECM formation in HSCs were investigated by reverse transcription polymerase chain reaction (RT-PCR) and western blotting assays. Naringenin reduced not only accumulation of ECM, including collagen Iα1 (Col Iα1), fibronectin (FN), and plasminogen activator inhibitor-1 (PAI-1), but also production of Smad3 induced by TGF-β1 in levels of mRNA and protein in a dose-dependent manner. These results provided obvious evidences that naringenin can directly or indirectly down-regulated Smad3 protein expression to exert anti-fibrogenic effects through intervening TGF-β1-Smad3 signaling pathway.
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