{"title":"Alginate oligosaccharides alleviate heat stress-induced damage to tight junctions and regulate autophagy in sertoli cells.","authors":"Wen-Feng Jiang, Tong Niu, Zheng-Hui Lan, Rong-Feng Cao, Kai-Qiang Fu, Zhong-Ling Jiang, Shi-Yong Zhu, Chun-Yu Xiong, Yan-Ni Feng, Hua-Tao Li","doi":"10.1071/RD26059","DOIUrl":null,"url":null,"abstract":"<p><strong>Context: </strong>Heat stress (HS) induces spermatogenic disorders and reduces sperm quality in males. Alginate oligosaccharides (AOS) exhibit antioxidant and reproductive protective effects, but the molecular mechanism by which AOS improves HS-induced declines in semen quality remains unclear.</p><p><strong>Aims: </strong>To investigate the protective effects and underlying molecular mechanism of AOS on HS-induced male reproductive impairment.</p><p><strong>Methods: </strong>Six-week-old mice were assigned to the following four groups: control, heat stress, AOS, and AOS + heat stress. We systematically evaluated male fertility, sperm quality, testicular morphology, blood-testis barrier (BTB), tight junctions in Sertoli cells (TJs), and autophagy levels.</p><p><strong>Key results: </strong>The results showed that AOS significantly attenuated the HS-induced reductions in pregnancy rate, litter size, sperm concentration, motility, and acrosome integrity. AOS also alleviated HS-induced testicular structural damage and blood-testis barrier leakage, and restored the expression levels of ZO-1, occludin, and claudin-11. In addition, HS induced abnormally elevated autophagy, as evidenced by increased autophagosomes, upregulated expression of LC3B, Beclin-1, and autophagy-related genes, and decreased p62 expression levels, whereas AOS restored autophagic flux to normal levels.</p><p><strong>Conclusions: </strong>The protective effects of AOS relieve heat stress-induced damage to tight junctions via regulating autophagy in Sertoli cells.</p><p><strong>Implications: </strong>These findings provide a theoretical basis for AOS as a potential agent for the prevention of HS-related reproductive disorders.</p>","PeriodicalId":516117,"journal":{"name":"Reproduction, fertility, and development","volume":"38 10","pages":""},"PeriodicalIF":2.1000,"publicationDate":"2026-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Reproduction, fertility, and development","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1071/RD26059","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Context: Heat stress (HS) induces spermatogenic disorders and reduces sperm quality in males. Alginate oligosaccharides (AOS) exhibit antioxidant and reproductive protective effects, but the molecular mechanism by which AOS improves HS-induced declines in semen quality remains unclear.
Aims: To investigate the protective effects and underlying molecular mechanism of AOS on HS-induced male reproductive impairment.
Methods: Six-week-old mice were assigned to the following four groups: control, heat stress, AOS, and AOS + heat stress. We systematically evaluated male fertility, sperm quality, testicular morphology, blood-testis barrier (BTB), tight junctions in Sertoli cells (TJs), and autophagy levels.
Key results: The results showed that AOS significantly attenuated the HS-induced reductions in pregnancy rate, litter size, sperm concentration, motility, and acrosome integrity. AOS also alleviated HS-induced testicular structural damage and blood-testis barrier leakage, and restored the expression levels of ZO-1, occludin, and claudin-11. In addition, HS induced abnormally elevated autophagy, as evidenced by increased autophagosomes, upregulated expression of LC3B, Beclin-1, and autophagy-related genes, and decreased p62 expression levels, whereas AOS restored autophagic flux to normal levels.
Conclusions: The protective effects of AOS relieve heat stress-induced damage to tight junctions via regulating autophagy in Sertoli cells.
Implications: These findings provide a theoretical basis for AOS as a potential agent for the prevention of HS-related reproductive disorders.