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热尼化物通过改变DNA甲基化来缓解人类肝细胞的过氧化诱导的亡

Xinyue Peng¹, Luyi Tan², Jia Song³

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

Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association

|November 8, 2023

概括

基尼胺 (GP) 显示出表观遗传活性,调节DNA甲基化以保护肝细胞免受亡. 这项研究揭示了GP GP.

科学领域:

表观遗传学在表观遗传学中,表观遗传学是指表观遗传学.
肝病学肝病学是一种肝病学.
分子生物学分子生物学

背景情况:

基尼化物 (GP) 是一种化合物,在肝细胞中具有已知的抗氧化和抗丧性质.
了解GP的安全极限和分子机制,特别是其表观遗传效应,至关重要.
过氧化 (H2O2) 用于诱导人类肝细胞 (L-02细胞) 中的氧化应激和亡.

研究的目的:

为了研究Geniposide (GP) 对人类肝细胞DNA甲基化的表观遗传效应.
阐明GP抑制H2O2诱导的亡的机制.
为了确定GP在L-02细胞中的生物安全暴露极限.

主要方法:

确定了GP在L-02细胞上的半抑制度 (IC50).
分析了全球DNA甲基化模式和DNA甲基转移酶 (DNMT1) 和脱甲基酶 (TET1,TET2) 的表达.
评估了GP对亡相关基因 (P53,Bcl-2,AKT) 的表达和促进者DNA甲基化的影响.

主要成果:

在正常L-02细胞上,GP的IC50为57.7 mg/mL.
GP (900μg/mL) 表现出表观遗传活性,增加DNMT1和减少TET1/TET2表达,从而增强全球DNA甲基化.
GP逆转了H2O2诱导的P53,Bcl-2和AKT水平的变化,并减少了AKT和Bcl-2的促进物甲基化,抑制了亡.

结论:

基尼胺调节全球DNA甲基化和特定基因表达 (P53,Bcl-2,AKT),以抑制人类肝细胞的亡.
总理证明了表观遗传效应,这有助于其对抗氧化应激诱导的肝细胞死亡的保护作用.
这些发现为Geniposide的安全评估和治疗潜力提供了新的理论参考.

关键词:

细胞灭亡 (apoptosis) 是一种死亡的过程.通过DNA甲基化.基因化物是一种基因化物.肝细胞肝细胞过氧化是一种过氧化.

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