Melatonin alleviates LPS‐induced endoplasmic reticulum stress and inflammation in spermatogonial stem cells. Issue 5 (29th September 2020)

• Record Type: Journal Article
• Authors: Yang, Donghui; Wei, Yudong; Lu, Qizhong; Qin, Dezhe; Zhang, Mengfei; Du, Xiaomin; Xu, Wenjing; Yu, Xiuwei; He, Chen; Li, Na; Peng, Sha; Li, Guangpeng; Hua, Jinlian
• Is Part Of: Journal of cellular physiology. Volume 236:Issue 5(2021)
• Page Start: 3536
• Page End: 3551
• Publication Date: 2020-09-29
• Subjects: endoplasmic reticulum stress -- inflammatory responses -- lipopolysaccharide -- melatonin -- SSC; Physiology -- Periodicals; Cell physiology -- Periodicals; 571.6
• DOI: 10.1002/jcp.30088
• Languages: English
• ISSNs: 0021-9541

Abstract

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. Abstract : 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.