Document Type : Original Article
Authors
1
Department of Clinical Science, Faculty of Veterinary Medicine, University of Tabriz, Tabriz, Iran
2
University of Tabriz
3
Medical Technology Research Center, Institute of Health Technology, Kermanshah University of Medical Sciences, Kermanshah, Iran
4
Cellular and Molecular Research Center, Basic Health Sciences Institute, Shahrekord University of Medical Sciences, Shahrekord, Iran
5
Cancer and Immmunology Research Center, Research Institute for Health Development, Kurdistan University of Medical Science, , Iran
6
Faculty of Medicine, Tabriz University of Medical Science, Tabriz, Iran
7
Department of Clinical Science, Faculty of Veterinary Medicine, University of Tabriz, Tabriz, Iran.
10.30466/vrf.2024.2039638.4415
Abstract
This study aimed to explore whether melatonin protects TM3 Leydig cells from CoCl2-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-1; Group 2), a group treated with cobalt (II) chloride (CoCl2, 100.00 µM) to induce hypoxia (Group 3), and a melatonin + CoCl2 group (Group 4). After 96 hr of incubation, cell viability was assessed using the MTT assay, and TGF-β1, Alk5, and Bmp4 gene and protein expressions were measured through real-time PCR and western blotting. The CoCl2 and melatonin + CoCl2 groups exhibited significantly diminished cell viability compared to the control. However, melatonin treatment enhanced survival in the CoCl2-exposed cells. Notably, TGF-β1 expression was elevated in all groups. Alk5 gene and protein expression increased in CoCl2-treated groups but was lower in the melatonin + CoCl2 group. Melatonin treatment reduced Bmp4 expression compared to the control, while CoCl2 groups showed increased Bmp4 levels. These findings suggest melatonin's potential as a therapeutic agent against oxidative stress and hypoxia in TM3 cells through its antioxidant properties.
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