封堵器
内科学
内分泌学
促黄体激素
紧密连接
MAPK/ERK通路
精子
精子发生
分泌物
蛋白激酶A
生殖毒性
p38丝裂原活化蛋白激酶
激素
睾酮(贴片)
激酶
化学
男科
细胞生物学
生物
毒性
医学
作者
Jianhui Liu,Lihua Ren,Jialiu Wei,Jin Zhang,Yupeng Zhu,Xiangyang Li,Jing Li,Junchao Duan,Xianqing Zhou,Zhiwei Sun
摘要
Abstract Fine particle matter (PM) is correlated with male reproductive dysfunction in animals and humans, but the underlying mechanisms remain unknown. To investigate the toxic mechanism of PM, 32 male Sprague‐Dawley (SD) rats were exposed to saline or PM 2.5 with the doses of 1.8, 5.4, and 16.2 mg/kg.b.w. via intratracheal instillation, respectively, one time every 3 days, in total times for 30 days. Sperm concentration, hormone level, the expressions of BTB‐associated protein and the mitogen‐activated protein kinase (MAPK) pathway, tumor necrosis factor α and transforming growth factor β3 levels were detected. The results showed a decrease in sperm number, testosterone and luteinizing hormone levels and altered ultrastructure of BTB in testis of rat after exposure to PM 2.5 . The protein levels of N‐Cadherin, Occludin, Claudin‐11, and Connexin‐43 were significantly decreased in the testes. TGF‐β3 content in testes showed increase, with the p‐p38/p38 MAPK ratio also increasing after PM 2.5 exposure. These results demonstrate that PM 2.5 restrained the expressions of BTB‐associated proteins through activating TGF‐β3/p38 MAPK pathway and decreasing testosterone secretion, and therefore lead to the damage of BTB resulting in the decrease of sperm quality, which might be the potential reasons for its negative effects on spermatogenesis and male reproduction.
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