Cadmium (Cd) is a frequent environmental pollutant associated with biological toxicity that can harm female reproduction. Anthocyanins have been reported to reduce the toxicity of Cd. In the present study, the protective effects and underlying mechanisms of malvidin-3-O-glucoside (M3G) against the toxicity of Cd on female reproduction in KGN cells (human ovarian granulosa-like tumor cells) were investigated. After treating cells with 10 µmol/L cadmium chloride, the results showed that M3G lessened Cd-induced KGN cell cytotoxicity better than malvidin and malvidin-3,5-O-diglucoside. Additionally, M3G significantly decreased the Cd-induced generation of reactive oxygen species, inhibited the Cd-induced arrest of the G2/M phase of the cell cycle, and increased estradiol (E2) production. According to transcriptomic results, M3G reduced the abnormal expression of genes that responded to estrogen. Additionally, M3G promoted the endogenous synthesis and secretion of E2 by controlling the expression of CYP17A1 and HSD17B7. The current findings indicated that M3G is of great potential to prevent Cd-induced female reproductive impairment as a dietary supplement.

中文翻译：

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Malvidin-3-O-Glucoside 可改善镉介导的人颗粒细胞雌二醇生成中的细胞功能障碍

镉 (Cd) 是一种常见的环境污染物，具有生物毒性，可损害女性生殖。据报道，花青素可以降低镉的毒性。在本研究中，研究了 Malvidin-3-O-glucoside (M3G) 对 Cd 对 KGN 细胞（人卵巢颗粒样肿瘤细胞）雌性生殖毒性的保护作用和潜在机制。用10 µmol/L氯化镉处理细胞后，结果表明M3G比malvidin和malvidin-3,5-O-diglucoside更好地减轻Cd诱导的KGN细胞的细胞毒性。此外，M3G 显着减少 Cd 诱导的活性氧的产生，抑制 Cd 诱导的细胞周期 G2/M 期停滞，并增加雌二醇 (E2) 的产生。根据转录组结果，M3G 减少了对雌激素有反应的基因的异常表达。此外，M3G通过控制CYP17A1和HSD17B7的表达促进E2的内源合成和分泌。目前的研究结果表明，M3G 作为膳食补充剂在预防镉引起的女性生殖障碍方面具有巨大潜力。