Testosterone Protects Pancreatic β-cells from Apoptosis and Stress-Induced Accelerated Senescence
Androgens are steroid hormones that are very important in the sexual development and the maintenance of male reproductive system, and also have diverse actions in non-reproductive tissues, including potent antioxidant capacity. Type 2 diabetes mellitus is caused by tissue insulin resistance and insu...
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Published in | The world journal of men's health Vol. 39; no. 4; pp. 724 - 732 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
Korea (South)
Korean Society for Sexual Medicine and Andrology
01.10.2021
대한남성과학회 |
Subjects | |
Online Access | Get full text |
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Summary: | Androgens are steroid hormones that are very important in the sexual development and the maintenance of male reproductive system, and also have diverse actions in non-reproductive tissues, including potent antioxidant capacity. Type 2 diabetes mellitus is caused by tissue insulin resistance and insufficient insulin secretion from the pancreatic β-cells. The progressive decline of pancreatic β-cells in diabetes is closely related with the severity of disease. We wanted to know whether dihydrotestosterone (DHT) can protect insulin secreting pancreatic β-cells from apoptosis and accelerated senescence induced by oxidative stress.
Cultured INS-1 cells were used. Various concentrations of H₂O₂ were applied to exert oxidative stresses. The degrees of apoptosis, accelerated senescence, and the changes of the expressions of related signaling molecules after the application of DHT were analyzed by CCK-8, p16 expression, SA-β-Gal staining, reverse transcription polymerase chain reactions and Western blots.
The application of H₂O₂ significantly increased (p<0.05) the degree of senescence and apoptosis of cultured INS-1 β-cells. DHT not only showed anti-oxidant protective capacity, but also significantly reduced (p<0.05) the degree of accelerated senescence.
DHT effectively protects pancreatic islet INS-1 β-cells from H₂O₂ induced oxidative stress. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 2287-4208 2287-4690 |
DOI: | 10.5534/WJMH.200169 |