Effects of melatonin on the mitogen-activated protein kinase signaling genes in hypoxic Leydig cells

Leydig cells play a crucial role in male reproductive physiology, and their dysfunction is often associated with male infertility. Hypoxia negatively affects the structure and function of Leydig cells. This study aimed to investigate the impact of melatonin on the c-Jun N-terminal kinase (Jnk), P۳۸, and extra-cellular signal-regulated kinases ۱ and ۲ (Erk۱/۲) mitogen-activated protein kinase (MAPK) signaling pathways in TM۳ mouse Leydig cells under hypoxia induced by cobalt (II) chloride (CoCl۲). The TM۳ cell line was utilized as a subject of research, and ۱۰۰ μM CoCl۲ was employed to induce hypoxia. Following the addition of ۱۰.۰۰ ng mL-۱ melatonin, quantitative reverse transcription-polymerase chain reaction and western blot analyses were conducted to assess the gene expression and protein level of Jnk, p۳۸, and Erk۱/۲, while enzyme-linked immunosorbent assay was used to measure testosterone secretion. The results showed that melatonin significantly increased testosterone production in the CoCl۲ + melatonin group compared to the CoCl۲-treated group. Furthermore, melatonin elevated both the protein level and mRNA expression of Erk۱/۲, Jnk, and p۳۸ genes in the CoCl۲ + melatonin group compared to the CoCl۲ group. In conclusion, melatonin activated the Jnk, p۳۸, and Erk۱/۲ MAPK signaling pathways and enhanced testosterone production in the presence of CoCl۲ in TM۳ cells.

کلیدواژه ها:

Hypoxia ، Leydig cells ، Melatonin ، mitogen-activated protein kinase ، Signal Transduction