Melatonin alleviates LPS‐induced endoplasmic reticulum stress and inflammation in spermatogonial stem cells
Orchitis is one of the leading causes of male animal infertility and is associated with inflammatory reactions caused by the bacterium. It has been reported that there is a mutual coupling effect between endoplasmic reticulum stress (ERS) and inflammatory response. Our studies showed that lipopolysa...
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Published in | Journal of cellular physiology Vol. 236; no. 5; pp. 3536 - 3551 |
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Main Authors | , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
Wiley Subscription Services, Inc
01.05.2021
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Subjects | |
Online Access | Get full text |
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Summary: | Orchitis is one of the leading causes of male animal infertility and is associated with inflammatory reactions caused by the bacterium. It has been reported that there is a mutual coupling effect between endoplasmic reticulum stress (ERS) and inflammatory response. Our studies showed that lipopolysaccharide (LPS) could cause testicular damages, apoptosis, ERS, and inflammatory responses in spermatogonial stem cells (SSCs); ERS‐related apoptosis proteins were activated and the expression of ERS genes was significantly upregulated; meanwhile, the expression of Toll‐like receptor 4 and inflammation factors was apparently increased with LPS treatment. Moreover, melatonin (MEL) could rescue testicular damage, and significantly inhibited the expression of ERS‐related apoptosis genes, ERS markers, and inflammatory factors in SSCs and MEL played repairing and anti‐infection roles in LPS‐induced testicular damage. Therefore, MEL may be used as a drug to prevent and control bacterial infections in male reproductive systems. However, the specific molecular mechanism of MEL to resist ERS and inflammatory response remains to be further studied.
Melatonin (MEL) could play a significant role in lipopolysaccharide (LPS)‐induced endoplasmic reticulum stress (ERS) and inflammatory responses in spermatogonial stem cells (SSCs). LPS could cause testicular damage and induce apoptosis, ERS, and inflammatory responses in SSCs, while exogenous MEL can inhibit the expression of ERS‐related apoptosis marker genes and inflammatory factors, at the same time, exogenous MEL could also alleviate testicular damage caused by LPS. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0021-9541 1097-4652 |
DOI: | 10.1002/jcp.30088 |