细胞凋亡
自噬
细胞生物学
间质细胞
生物
流式细胞术
半胱氨酸蛋白酶3
活力测定
程序性细胞死亡
化学
分子生物学
内分泌学
生物化学
激素
促黄体激素
作者
Qianru Zhang,Jason William Grunberger,Nitish Khurana,Xin Zhou,Xianyu Xu,Hamidreza Ghandehari,Fenglei Chen
出处
期刊:Cells
[MDPI AG]
日期:2022-06-07
卷期号:11 (12): 1863-1863
被引量:2
标识
DOI:10.3390/cells11121863
摘要
Accumulation of silica nanoparticles (SNPs) in the testes leads to male reproductive toxicity. However, little is known about the effect and mechanistic insights of SNP-induced autophagy on apoptosis in Leydig cells. In this study, we aimed to verify the role of SNP-induced autophagy in apoptosis and explore the possible underlying mechanism in mouse primary Leydig cells (PLCs). H&E staining showed that SNPs changed the histological structures of the testes, including a reduction in the Leydig cell populations in vivo. CCK-8 assay showed that SNPs decreased cell viability, and flow cytometry showed that SNPs increased cell apoptosis, both in a dose-dependent manner in vitro. Additionally, Western blotting further found that SNPs activated autophagy by an increase in BECLIN-1, ATG16L, and LC3-II levels and promoted the intrinsic pathway of apoptosis by an increase in the BAX/BCL-2 ratio, cleaved the caspase 8 and caspase 3 levels. Furthermore, autophagy decreased SNP-induced apoptosis via regulation of the caspase 8 level combined with rapamycin, 3-methyladenine, and chloroquine. BECLIN-1 depletion increased the caspase 8 level, leading to an increase in SNP-induced cell apoptosis. Collectively, this evidence demonstrates that SNPs activated BECLIN-1-mediated autophagy, which prevented SNP-induced testicular toxicity via the inhibition of caspase 8-mediated cell apoptosis in Leydig cells.
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