Molecular mechanisms of melatonin in the reversal of LPS-induced EMT in peritoneal mesothelial cells.

Peritoneal dialysis (PD)-associated peritoneal fibrosis is a serious complication in patients with chronic renal failure on dialysis maintenance. Studies have shown that patients on long‑term PD have chronic inflammation. The epithelial-to-mesenchymal transition (EMT) induced by inflammation is a major cause of peritoneal fibrosis and dysfunction. As a potent antioxidant property, melatonin has an antifibrotic effect. The present study investigated the effects of melatonin on lipopolysaccharide (LPS)‑induced EMT and examined the molecular mechanisms in peritoneal mesothelial cells using western blotting, reverse transcription‑polymerase chain reaction and immunofluorescence staining. The results of the study found that melatonin inhibited LPS‑induced morphological changes, decreased the expression of LPS-induced markers of EMT, including vimentin and α‑smooth muscle actin, and increased the expression of E‑cadherin. In addition, it was found that the action of melatonin was mediated through the inactivation of the Toll‑like receptor (TLR)4/c‑Jun N‑terminal kinase and TLR4/nuclear factor‑κB‑Snail signaling pathways. Thus, these data provided novel insight into the mechanisms underlying the function of melatonin in peritoneal mesothelial cells during the processes of EMT, and may provide a theoretical basis for the treatment of peritoneal fibrosis.