Reproduction, fertility, and development · 2026
Alginate oligosaccharides alleviate heat stress-induced damage to tight junctions and regulate autophagy in sertoli cells.
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Jiang Wen-Feng, Niu Tong, Lan Zheng-Hui, Cao Rong-Feng, Fu Kai-Qiang, Jiang Zhong-Ling, Zhu Shi-Yong, Xiong Chun-Yu, Feng Yan-Ni, Li Hua-Tao
Аннотация
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.
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.