解剖学杂志2025，Vol.48Issue(3)：192-198,7.DOI:10.3969/j.issn.1001-1633.2025.03.002
褪黑素通过褪黑素受体1抑制RSL3诱导的AML12细胞铁死亡
Melatonin mitigates RSL3-induced ferroptosis in AML12 cells via melatonin receptor 1
摘要
Abstract
Objective:To investigate whether melatonin can alleviate ferroptosis induced by RAS-selective lethal small molecule 3(RSL3)in AML12 cells and the role of melatonin receptor 1(MT1)in the process.Methods:A ferroptosis model of AML12 cells was established via RSL3 induction.Cell viability was assessed by CCK-8 staining.Intracellular ferrous ion(Fe2+),reactive oxygen species(ROS),and lipid peroxidation levels were detected through fluorescent probe staining.Expressions of MT1 and ferroptosis-related proteins,namely long-chain acyl-CoA synthetase 4(ACSL4)and glutathione peroxidase 4(GPX4),were measured by Western blotting.The impact of MT1 knockdown on the effects of melatonin was observed using the broad-spectrum receptor antagonist of melatonin,N-acetyl-2-benzyltryptamine(Luz)and small RNA interference technology.Results:After RSL3 induction,AML12 cell viability decreased,GPX4 expression was reduced,and ACSL4 expression was increased,along with elevated levels of intracellular Fe2+,ROS,and lipid peroxidation.Melatonin pretreatment antagonized the changes in cell viability,ferroptosis-related proteins,intracellular Fe2+,ROS,and lipid peroxidation.RSL3 induction led to a decrease in MT1 expression in AML12 cells,which was rescued by melatonin administration.Luz and MT1 knockdown could both antagonize the protective effect of melatonin on AML12 cell ferroptosis.Conclusion:Melatonin may alleviate RSL3-induced ferroptosis in AML12 cells via MT1.关键词
肝细胞/铁死亡/褪黑素/褪黑素受体/缺血再灌注损伤/Ras选择性致死小分子3Key words
hepatic cell/ferroptosis/melatonin/melatonin receptor/ischemia-reperfusion injury/RAS-selective lethal small molecule 3分类
医药卫生引用本文复制引用
褚芳芳,齐春惠,张月霞,范佳琦,于树娜,肖培伦,蒋吉英..褪黑素通过褪黑素受体1抑制RSL3诱导的AML12细胞铁死亡[J].解剖学杂志,2025,48(3):192-198,7.基金项目
山东省自然科学基金(ZR2022MH011) （ZR2022MH011）
山东省医药卫生科技发展计划项目(202001020642) （202001020642）
