作者
Wen-Feng Jiang,Tong Niu,Zheng-Hui Lan,Rongfeng Cao,Kai-Qiang Fu,Jiang Zhong-ling,Shi‐Yong Zhu,Chun-Yu Xiong,Yanni Feng,Hua-Tao Li
摘要
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.