Ecotoxicology and environmental safety · 2025
Alleviating effect of ellagic acid on ovarian reserve function injury induced by zearalenone and its mechanism.
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Zhao Jiafu, Pan Zhiren, Wen Xiaoyan, Zhang Wei, Chen Yi, Zhang Xilu, Lu Qingmei, Liu Bin, Zhou Mingshuai, Chen Xiang, Shi Xiaoli
Аннотация
PURPOSE: Zearalenone (ZEA), a widespread mycotoxin, harms reproductive health in humans and animals. Ellagic acid (EA), a plant-derived polyphenol, can reduce such damage. This study explores how EA helps repair ZEA's effects on goat ovarian granulosa cells (OGCs) and murine ovarian.
METHODS: The detoxifying effects of EA on ZEA were examined both in vitro and in vivo.
PRINCIPAL RESULTS: In Vitro Studies: EA ameliorated ZEA-induced oxidative stress, mitochondrial dysfunction, and apoptosis in OGCs. Specifically, EA downregulated the expression of endoplasmic reticulum stress (ERS) genes (ERN1, XBP1, ATF6), reduced ROS and MDA levels, while restoring SOD and T-AOC to control levels. Furthermore, EA upregulated mitochondrial function genes (ATP5A1, CLPP) and restored mitochondrial membrane potential (MMP). Concurrently, EA downregulated the expression of apoptosis-associated proteins (caspase-9, caspase-3), elevated PCNA protein expression, Bcl-2/Bax ratio, and ultimately reduced the cellular apoptosis rate. Additionally, EA mitigated ZEA-induced estrogen secretion dysfunction in OGCs by downregulating ZEA-elevated E2 synthesis-related proteins (3β-HSD, CYP17A1), the estrogen receptor gene (ESR1) expression, and E2 secretion levels.
IN VIVO STUDIES: EA alleviated ZEA-induced oxidative damage and reproductive toxicity in mice. Treatment with EA elevated ZEA-reduced levels of IL-10, T-SOD, and GPX. Conversely, EA reduced ZEA-elevated levels of MDA, TNF-α, and key reproductive hormones (GnRH, LH, FSH, E2, P4).
CONCLUSIONS: The collective results of in vitro and in vivo experiments demonstrate that ZEA exerts significant detrimental effects on reproductive cells and ovarian function by inducing oxidative stress, ERS, diminishing mitochondrial function, and disrupting sex hormone secretion. EA alleviates these ZEA-induced toxic effects.
METHODS: The detoxifying effects of EA on ZEA were examined both in vitro and in vivo.
PRINCIPAL RESULTS: In Vitro Studies: EA ameliorated ZEA-induced oxidative stress, mitochondrial dysfunction, and apoptosis in OGCs. Specifically, EA downregulated the expression of endoplasmic reticulum stress (ERS) genes (ERN1, XBP1, ATF6), reduced ROS and MDA levels, while restoring SOD and T-AOC to control levels. Furthermore, EA upregulated mitochondrial function genes (ATP5A1, CLPP) and restored mitochondrial membrane potential (MMP). Concurrently, EA downregulated the expression of apoptosis-associated proteins (caspase-9, caspase-3), elevated PCNA protein expression, Bcl-2/Bax ratio, and ultimately reduced the cellular apoptosis rate. Additionally, EA mitigated ZEA-induced estrogen secretion dysfunction in OGCs by downregulating ZEA-elevated E2 synthesis-related proteins (3β-HSD, CYP17A1), the estrogen receptor gene (ESR1) expression, and E2 secretion levels.
IN VIVO STUDIES: EA alleviated ZEA-induced oxidative damage and reproductive toxicity in mice. Treatment with EA elevated ZEA-reduced levels of IL-10, T-SOD, and GPX. Conversely, EA reduced ZEA-elevated levels of MDA, TNF-α, and key reproductive hormones (GnRH, LH, FSH, E2, P4).
CONCLUSIONS: The collective results of in vitro and in vivo experiments demonstrate that ZEA exerts significant detrimental effects on reproductive cells and ovarian function by inducing oxidative stress, ERS, diminishing mitochondrial function, and disrupting sex hormone secretion. EA alleviates these ZEA-induced toxic effects.