Hepatoprotective effects of silybin in liver fibrosis

Abstract

Chronic liver disease results in a response resembling "wound healing", also known as fibrosis, resulting in the progressive accumulation of connective tissue. Excessive fibrogenesis that results in the disruption of intercellular connections, interactions, and extracellular matrix composition are features of the fibrotic process mediated by various cell types and chemical mediators such as transforming growth factor-β. Redox-sensitive processes are major contributors to controlling this inflammatory and pro-fibrogenic cytokine's production and synthesis. Other essential hepatic fibrogenesis activities, such as the activation of stellate cells, the expression of metalloproteinases and their inhibitors can also be linked to generation of reactive oxygen species and lipid peroxidation products, which are implicated in development and progression of fibrosis. The herb Silybum marianum, also known as milk thistle, is widely studied for its potential to treat liver illnesses. Silymarin contains 50% to 70% silybin, which has the highest level of biological activity. In comparison, silybin seems to be relatively safer and the available evidence on its potential mechanisms of action is encouraging. The aim of this article is to analyze the increasing evidences linking biochemical oxidative events to excessive fibrogenesis and silybin's inhibitory mechanisms that aid in the reversal of fibrosis and fibrotic lesions.

Keywords: Fibrosis; Inflammation; Kupffer cells; Liver; Silybin

Core Tip: Liver fibrosis, a wound-healing response to chronic hepatic injury, is driven by redox-sensitive pathways, reactive oxygen species, and pro-fibrogenic cytokines like transforming growth factor-β. Silybum marianum (milk thistle), particularly its active compound silybin, exhibits promising antioxidant and anti-fibrotic properties. This study explores the biochemical oxidative mechanisms behind fibrogenesis and highlights silibin’s potential in reversing liver fibrosis through inhibition of oxidative stress and fibrogenic signaling pathways.