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Published on: July 24, 2018
Melatonin alleviates LPS-induced endoplasmic reticulum stress and inflammation in spermatogonial stem cells
Donghui Yang1, Yudong Wei1, Qizhong Lu1
1Shaanxi Centre of Stem Cells Engineering and Technology, College of Veterinary Medicine, Northwest A&F University, Yangling, Shaanxi, China.
Abstract:
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.
Insights
Melatonin (MEL) protects male reproductive cells from bacterial infection damage by reducing endoplasmic reticulum stress (ERS) and inflammation. This suggests MEL could be a potential therapeutic for male infertility caused by bacterial infections.
Area of Science:
- Reproductive Biology
- Immunology
- Cellular Stress Response
Background:
- Orchitis, a bacterial infection, is a primary cause of male infertility.
- Endoplasmic reticulum stress (ERS) and inflammatory responses are interconnected and contribute to testicular damage.
- Lipopolysaccharide (LPS) exposure induces testicular damage, apoptosis, ERS, and inflammation in spermatogonial stem cells (SSCs).
Purpose of the Study:
- To investigate the protective effects of melatonin (MEL) against LPS-induced testicular damage in SSCs.
- To elucidate the role of MEL in modulating ERS and inflammatory responses in the context of bacterial infection.
- To explore the potential of MEL as a therapeutic agent for male reproductive tract infections.
Main Methods:
- Treatment of SSCs with LPS to induce testicular damage, ERS, and inflammation.
- Administration of MEL to assess its protective and therapeutic effects.
- Analysis of gene and protein expression related to ERS, apoptosis, and inflammation (e.g., Toll-like receptor 4).
Main Results:
- LPS treatment significantly upregulated ERS genes, activated ERS-related apoptosis proteins, and increased inflammation factors in SSCs.
- MEL treatment rescued testicular damage induced by LPS.
- MEL significantly inhibited the expression of ERS-related apoptosis genes, ERS markers, and inflammatory factors, demonstrating repairing and anti-infective properties.
Conclusions:
- Melatonin exhibits protective effects against bacterial-induced testicular damage by mitigating endoplasmic reticulum stress and inflammation.
- MEL demonstrates potential as a therapeutic agent for preventing and treating bacterial infections in the male reproductive system.
- Further research is needed to fully understand the molecular mechanisms underlying MEL's anti-ERS and anti-inflammatory actions.
