[Research progress on the quercetin target role and signaling pathway in anti-liver fibrosis]

Hepatic fibrosis is a common chronic liver disease, and its pathogenesis and influencing factors exhibit diverse characteristics. Pharmacological intervention is currently the main therapeutic approach for hepatic fibrosis. Quercetin is a flavonoid compound with multiple biological activities, which can inhibit inflammatory responses, reduce oxidative stress, suppress hepatic stellate cell activation and excessive collagen deposition, and regulate hepatic lipid metabolism, thus exerting anti-hepatic fibrosis effects. Quercetin delays the progression of fibrosis via regulating signaling pathways such as Rac1/NOX1 and transforming growth factor-β1/Smad, thereby diminishing the activity of hepatic stellate cells and their accumulation in the extracellular matrix. Quercetin can also enhance the activity of antioxidant enzymes (such as superoxide dismutase and glutathione peroxidase) and reduce the damage of oxidative free radicals to hepatocytes by regulating the nuclear factor E2-related factor 2/antioxidant response element signaling pathway. Furthermore, it can inhibit the activation of the Toll-like receptor 4/nuclear factor-κB pathway and reduce the expression of pro-inflammatory factors, thus alleviating the inflammatory response. Concurrently, quercetin plays an active role in terms of regulating liver lipid metabolism, reducing abnormal lipid accumulation, and lessening the burden on hepatocytes. The multi-target and multi-pathway functional properties of quercetin render it highly promising in alleviating the pathological progression of liver fibrosis. This article summarizes the signaling pathways and target roles of quercetin in the treatment of liver fibrosis, providing an important reference for clinical intervention strategies and novel drug research and development.