Cigarette smoke exposure stimulates prostatic fibrosis and the potential protective functions of green tea epigallocatechin-3-gallate via regulating Hedgehog pathway

[Display omitted] •Cigarette smoke (CS) exposure stimulates prostatic collagen deposition and fibrosis.•CS exposure provokes prostatic epithelial-mesenchymal transition (EMT).•CS exposure triggers prostatic Hedgehog (HH) pathway.•Impeding the HH pathway helpes to ameliorate CS-induced prostatic deficits.•EGCG attenuates CS-induced prostatic fibrosis by modulating EMT and HH pathway. Cigarettes consumption is popular all over the world. In the meantime, green tea is widely accepted for their health benefits. Epigallocatechin-3-gallate (EGCG) is the most abundant catechin in green tea. This study aimed to investigate the effects of cigarette smoke (CS) exposure on human prostate cells and rat prostate, as well as the potential protective functions of EGCG. The results suggested that chronic CS exposure stimulated prostatic epithelial-mesenchymal transition (EMT), collagen deposition and fibrosis. Down-regulation of the Hedgehog (HH) signaling pathway helped to ameliorate CS-induced prostatic deficits. Meanwhile, EGCG could exhibit strong anti-fibrosis effects on prostate. Its underlying mechanisms were related to modulate EMT and decrease the activity of HH signal pathway.