数字农科院2.0

Investigation into Bioactive Selenium Species and the Mechanism of Action Behind Selenium-Enriched Rapeseed Flowering Stalks Alleviating Cadmium-Induced Toxicity in Mouse Sertoli Cells

文献类型： 外文期刊

作者： 车华涛;;陆亦晴;;李彤;;方小丽;;王新发;;王汉中;;顿小玲;;陈振娜

关键词： selenium-enriched rapeseed; Cadmium; organic selenium; mouse Sertoli cells; RNA-Seq; mechanism

期刊名称： Antioxidants

ISSN：

年卷期： 2025 年

页码：

收录情况： SCIE（2025版）

摘要： Cadmium (Cd) is a recognized environmental contaminant, present in soil, water, and food, which has been reported to cause male reproductive damage in vivo and vitro. Selenium-enriched rapeseed flowering stalks exhibit protective effects against Cd-induced reproductive damage, yet the bioactive components and underlying mechanisms remain unclear. We optimized the process of obtaining the crude extract (CE) via single-factor experiments. Subsequent bioassay-guided fractionation identified the water extract (WE) as significantly more effective in alleviating Cd-induced cytotoxicity compared to the petroleum ether extract, ethyl acetate extract, and n-butanol extract. High-performance liquid chromatography–inductively coupled plasma mass spectrometry (HPLC-ICP-MS) analysis revealed that WE contained the highest contents of methylselenocysteine (MeSeCys) and selenocystine (SeCys2) among four fractions. Both MeSeCys and SeCys2 exhibited protective effects against Cd-induced cytotoxicity. To further elucidate the underlying mechanisms, network pharmacology, RNA-Seq, qPCR, and Western blotting analysis were employed. The results revealed that WE exhibited good free radical scavenging capabilities, and the protective mechanisms of WE, MeSeCys, and SeCys2 against Cd-induced cytotoxicity were related to a reduction in oxidative damage, the inhibition of the ERK/p38 MAPK signaling pathway, and the suppression of cell cycle arrest, inflammation, and apoptosis triggered by Cd exposure. Collectively, these findings suggest that selenium-enriched rapeseed flowering stalks may serve as a promising dietary supplement in the prevention of Cd-induced reproductive toxicity.

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