Role of selenoprotein M knockdown in the melatonin antagonism of nickel-induced apoptosis and endoplasmic reticulum stress in mouse heart  

作　　者：Xintong ZHANG Xiaoxue GAI Lihua XU Wenxue MA Qiaohan LIU Bendong SHI Cheng FANG Jingzeng CAI Ziwei ZHANG 

机构地区：[1]College of Veterinary Medicine,Northeast Agricultural University,Harbin 150030,China [2]Suihua Agricultural and Rural Bureau,Suihua 152000,China [3]College of Veterinary Medicine,Northeast Agricultural University,Harbin 150030,China4.Key Laboratory of the Provincial Education,Department of Heilongjiang for Common Animal Disease Prevention and Treatment,Northeast Agricultural University,Harbin 150030,China

出　　处：《Journal of Zhejiang University-Science B(Biomedicine & Biotechnology)》2023年第5期406-417,共12页浙江大学学报（英文版）B辑（生物医学与生物技术）

基　　金：supported by the Heilongjiang Provincial Natural Science Foundation for Outstanding Youth(No.YQ2021C021),China。

摘　　要：The aim of this study was to investigate the role of selenoprotein M(SelM)in endoplasmic reticulum stress and apoptosis in nickel-exposed mouse hearts and to explore the detoxifying effects of melatonin.At 21 d after intraperitoneal injection of nickel chloride(NiCl_(2))and/or melatonin into male wild-type(WT)and SelM knockout(KO)C57BL/6J mice,NiCl_(2)was found to induce changes in the microstructure and ultrastructure of the hearts of both WT and SelM KO mice,which were caused by oxidative stress,endoplasmic reticulum stress,and apoptosis,as evidenced by decreases in malondialdehyde(MDA)content and total antioxidant capacity(T-AOC)activity.Changes in the messenger RNA(mRNA)and protein expression of genes related to endoplasmic reticulum stress(activating transcription factor 4(ATF4),inositol-requiring protein 1(IRE1),c-Jun N-terminal kinase(JNK),and C/EBP homologous protein(CHOP))and apoptosis(B-cell lymphoma-2(Bcl-2),Bcl-2-associated X protein(Bax),Caspase-3,Caspase-9,and Caspase-12)were also observed.Notably,the observed damage was worse in SelM KO mice.Furthermore,melatonin alleviated the heart injury caused by NiCl_(2)in WT mice but could not exert a good protective effect in the heart of SelM KO mice.Overall,the findings suggested that the antioxidant capacity of SelM,as well as its modulation of endoplasmic reticulum stress and apoptosis,plays important roles in nickel-induced heart injury.

关 键 词：Selenoprotein M(SelM) Nickel chloride(NiCl_(2)) MELATONIN Apoptosis Mouse heart 

分 类 号：R114[医药卫生—卫生毒理学]