Curcumin Alleviates Bisphenol A-Induced Blood-Testis Barrier Disruption in Mice by Targeting Surfactant Protein B (SFTPB) to Suppress Oxidative Stress-Activated NLRP3 Inflammasome

姜黄素 炎症体 氧化应激 化学 双酚A 基因敲除 药理学 作用机理 氧化磷酸化 双酚S 炎症 受体 机制(生物学) 细胞生物学 内分泌干扰物 支持细胞 信号转导 双酚
作者
Hongwei Duan,Shanshan Yang,Longfei Xiao,Shuai Yang,Bin Jiang,Zihao Fang,Zhenxing Yan,Jian-Lin Zeng,Xiaofei MA,Weitao Dong,Ya Liu,Hongwei Duan,Shanshan Yang,Longfei Xiao,Shuai Yang,Bin Jiang,Zihao Fang,Zhenxing Yan,Jian-Lin Zeng,Xiaofei MA
出处
期刊:Journal of Agricultural and Food Chemistry [American Chemical Society]
卷期号:73 (46): 29874-29885
标识
DOI:10.1021/acs.jafc.5c11194
摘要

Bisphenol A (BPA), a globally prevalent industrial chemical, significantly harms the male reproductive health. Curcumin has anti-inflammatory, antioxidation, and antiapoptosis pharmacological properties, but the effect and mechanism of curcumin against BPA-induced testicular damage are still unknown. This study investigates the protective effect of curcumin against Bisphenol A (BPA)-induced blood-testis barrier (BTB) injury in mice. BPA exposure caused oxidative stress, activated the NOD-like receptor protein 3 (NLRP3) inflammasome in Sertoli cells, and disrupted BTB integrity. Curcumin treatment alleviated these effects by reducing oxidative stress and inhibiting NLRP3 activation. We identified Surfactant Protein B (SFTPB) as a key target, finding that curcumin directly interacts with and down-regulates it. Functionally, SFTPB knockdown mimicked curcumin's protection, while its overexpression exacerbated BPA-induced damage. Our findings demonstrate that curcumin mitigates BPA-induced testicular injury by targeting SFTPB to suppress the oxidative stress-NLRP3 pathway, revealing a novel mechanism for the therapeutic action of curcumin.
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