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基尼胺通过m6A修饰通过PI3K/AKT3/FOXO1减少了HK-2细胞中氧化应激诱导的亡

Wenli Cheng¹, Luyi Tan², Susu Yu²

¹Food Safety and Health Research Center, NMPA Key Laboratory for Safety Evaluation of Cosmetics, Guangdong Provincial Key Laboratory of Tropical Disease Research, School of Public Health, Southern Medical University, Guangzhou 510515, PR China; Department of Public Health and Preventive Medicine, School of Medicine, Jinan University, Guangzhou, Guangdong 510632, PR China.

International immunopharmacology

|March 20, 2024

概括

基尼化物 (GP) 通过调节N6-甲基氨酸 (m6A) RNA甲基化,减轻过氧化 (H2O2) 诱导的细胞亡. 这项研究揭示了GP GP.

科学领域:

细胞生物学细胞生物学
分子生物学分子生物学
生物化学生物化学

背景情况:

过氧化 (H2O2) 诱导氧化应激,导致细胞亡和功能障碍.
基尼化物 (GP) 是一种虹膜类化合物,具有抗炎,抗氧化和抗丧性质.
N6-甲基氨酸 (m6A) RNA甲基化在细胞过程中发挥作用,包括细胞亡和应激反应.

研究的目的:

为了研究基尼胺 (GP) 对人类脏-2 (HK-2) 细胞中H2O2诱导的亡的保护作用.
探索涉及N6-甲基氨酸 (m6A) RNA甲基化和PI3K/AKT3/FOXO1信号通路的潜在机制.

主要方法:

用H2O2和Geniposide (GP) 对待HK-2细胞.
评估了细胞活力,细胞亡率和细胞周期.
使用RT-qPCR和西白斑测量了m6A相关酶,PI3K/AKT3/FOXO1和SOD2的mRNA和蛋白质水平.
测量了全球m6A甲基转移酶活性和m6A含量.
使用MeRIP-qPCR来确定特定基因的m6A甲基化水平.

主要成果:

暴露于H2O2会导致G1细胞周期停止和细胞亡的增加,而GP治疗显著减少了这种情况.
与H2O2组相比,GP干预增加了全球m6ARNA甲基转移酶活性和m6A含量.
在GP治疗上调节了SOD2蛋白表达,同时降低了PI3K和FOXO1蛋白水平.
AKT3的m6A甲基化水平与其蛋白质水平呈负相关性.

结论:

基尼化物 (GP) 有效地减轻H2O2诱导的HK-2细胞细胞循环停止和细胞亡.
GP调节全球m6ARNA甲基化场景,并通过m6A修改调节PI3K/AKT3/FOXO1信号通路.
总理证明了作为治疗功能障碍与氧化应激相关的治疗剂的潜力.

关键词:

细胞灭亡 (apoptosis) 是一种死亡的过程.基因化物是一种基因化物.在HK-2单元中,HK-2是单元.过氧化是一种过氧化.m6A甲基化的情况.

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