Hepatorenal complications in bleomycin-induced pulmonary fibrosis: a comprehensive review on its biochemical mechanisms and prophylactic considerations

Abstract

Bleomycin induced pulmonary fibrosis (PF) has been one of the most habituated experimental models in idiopathic PF (IPF) exploration since the 1970s. The bleomycin model is a classic model of lung toxin. Though utmost of the studies established lung part, its dangerous goods on the liver and kidneys are still under explored. The applicable studies were searched on PubMed, Web of Science, and Google Scholar using the keywords “bleomycin”, “pulmonary fibrosis”, “hepatorenal toxin”, “oxidative stress”, “nephroprotection”, “liver injury”, “order injury”, “Nrf2 activators”, and “factory-deduced antioxidants” published in 2017-2024." Substantiation from these studies showed that bleomycin treatment significantly raises the situations of serum biochemical labels, like alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (peak), creatinine, and blood urea nitrogen (BUN). Increase in all biochemical labels suggest serious damage to the liver and kidneys. Studies have shown that the main mechanisms involved in this toxin are oxidative stress (ROS), mitochondrial dysfunction, activation of seditious cytokines and TGF-β1/Smad signalling. Curcumin, quercetin, silymarin and resveratrol are among factory- deduced bioactive composites which displayed promising defensive parcels These effects are suggestively through their antioxidant, anti-inflammatory, and antifibrotic conduct. These findings punctuate the need to consider and pierce multiple organs in bleomycin studies to make experimental fibrosis exploration more applicable systemically. Herbal antioxidants and Nrf2 activators can offer effective forestalment against liver and renal damage caused by bleomycin.