Bicyclol: A Useful Agent for Silicosis?

Silicosis is one of the most prevalent occupational diseases worldwide, resulting from prolonged exposure to crystalline silica (SiO2). This exposure leads to persistent inflammation, lung fibrosis, and ultimately significant loss of lung function and death. Although the precise mechanisms remain unclear, the primary molecular pathogenesis of silicosis—ranging from SiO2-induced chronic inflammation to irreversible pulmonary fibrosis—shares considerable overlap with fibrosis mechanisms in various organs, including the secretion of inflammatory cytokines, the activation of fibrosis-related signaling pathways, and ferroptosis. Currently, there is no cure for silicosis; anti-fibrotic treatments are recommended to slow disease progression. Bicyclol, a hepatoprotective agent commonly used to manage elevated aminotransferases due to chronic hepatitis, has garnered attention in recent years for its anti-inflammatory and anti-fibrotic properties in organs such as the liver, heart, and kidney. It significantly reduces extracellular matrix (ECM) synthesis and deposition in these organs, thereby decelerating fibrosis progression. In the context of silicosis, bicyclol has demonstrated promising effects on both chronic inflammation and fibrosis, indicating its potential as a clinical treatment for silicosis. This review summarizes the effects of bicyclol during the chronic inflammation and fibrosis stages of silicosis progression, providing both direct and indirect evidence for its potential therapeutic application in silicosis management. However, it is worth noting that there is limited direct evidence specific to silicosis, and the current prospects mainly stem from indirect evidence of anti-fibrotic effects in other organs. There is still a long way to go before bicyclol truly becomes an approved drug for silicosis.