泽拉伦通过ROS介导的PI3K/AKT通路抑制哺乳能力
Hong Chen1, Di Qiu1, Xue Miao1
1College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, China.
Animals : an open access journal from MDPI
|April 12, 2025
概括
泽拉伦 (ZEA) 菌类毒素通过破坏乳腺并通过ROS介导的PI3K/AKT通路诱导亡,损害哺乳期. 这突出了管理ZEA污染影响的潜在目标.
科学领域:
- 毒理学 毒理学 毒理学
- 细胞生物学 细胞生物学
- 内分泌学 在内分泌学.
背景情况:
- 泽拉伦 (ZEA) 是食品和料中常见的真菌毒素,对乳腺功能和哺乳产生不明确的影响.
- 了解ZEA的影响对于食品安全和公共卫生至关重要,特别是对于哺乳期的表现.
研究的目的:
- 在体内和体外研究Zeaaralenone (ZEA) 对乳腺损伤和哺乳的影响.
- 阐明酸丁醇3-酶/蛋白酶B (PI3K/AKT) 信号通路在ZEA诱导的细胞反应中的作用.
- 探索反应性氧物种 (ROS) 在ZEA的作用机制中的参与.
主要方法:
- 哺乳小鼠和牛乳腺上皮细胞 (MAC-T) 暴露于不同剂量的ZEA.
- 乳腺损伤的评估是使用血素和欧 (HE) 染色和CSNK免疫光检测.
- 用PCNA免疫组织化学和TUNEL染色来评估细胞增殖和细胞亡.
- 在MAC-T细胞中分析了PI3K/AKT信号传递,氧化应激和 κ-素 (CSNK) 表达.
- 研究了ROS清除剂 (NAC) 和PI3K/AKT激活剂 (740-Y-P) 的作用.
主要成果:
- 在小鼠和后代的体重增加中,ZEA暴露减少了哺乳期,这表明体内毒性.
- ZEA诱导了乳腺损伤,减少了增殖,并促进了乳腺组织的亡.
- 在体外,ZEA抑制了MAC-T细胞的增殖,增加了亡和氧化应激,并抑制了PI3K/AKT信号和CSNK的表达.
- NAC和740-Y-P治疗逆转了ZEA诱导的细胞损伤,NAC恢复了PI3K/AKT活性.
结论:
- 通过ROS介导的PI3K/AKT通路的抑制,ZEA诱导了细胞亡并破坏了MAC-T细胞的增殖.
- ZEA 损害了哺乳功能,可能是由于对乳腺上皮细胞的直接毒性.
- 准ROS-PI3K/AKT通路可能为减轻ZEA对哺乳期的不良影响提供策略.
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