Protective effects of melatonin against hypoxia-induced TM3 cell damage via suppression of the TGF-β pathway

Source: PubMed Central Open Access, NCBI / U.S. National Library of Medicine

This study aimed to explore whether melatonin protects TM3 Leydig cells from cobalt (II) chloride (CoCl)-induced hypoxia through the transforming growth factor beta (TGF-β) signaling pathway. Cells were divided into four groups: a control group without treatment (Group 1), a melatonin group (10.00 ng mL; Group 2), a group treated with CoCl(100 µM) to induce hypoxia (Group 3), and a melatonin + CoClgroup (Group 4). After 96 hr of incubation, cell viability was assessed using the MTT assay, and,, andgene and protein expressions were measured through RT‑PCR and western blotting. The CoCland melatonin + CoClgroups exhibited significantly diminished cell viability compared to the control. However, melatonin treatment enhanced survival in the CoCl-exposed cells. Notably, transforming growth factor beta 1 expression was elevated in all groups.gene and protein expression increased in CoCl-treated groups but was lower in the melatonin + CoClgroup. Melatonin treatment reduced bone morphogenetic protein 4 expression compared to the control, while CoClgroups showed increased bone morphogenetic protein 4 levels. These findings suggest melatonin's potential as a therapeutic agent against oxidative stress and hypoxia in TM3 cells through its antioxidant properties.