中国医科大学学报2025，Vol.54Issue(4)：289-294,6.DOI:10.12007/j.issn.0258-4646.2025.04.001
右美托咪定通过核因子κB缓解阿霉素诱导的心肌损伤
Dexmedetomidine attenuates doxorubicin-induced myocardial injury through nuclear factor κB
摘要
Abstract
Objective To explore the mechanism through which dexmedetomidine(Dex)alleviates doxorubicin(Adr)-induced myo-cardial injury via regulating nuclear factor κB(NF-κB)expression.Methods Sprague-Dawley rats were divided into control,Adr,and Adr+Dex groups.Theirs hearts were harvested for hematoxylin and eosin(HE)staining,immunohistochemical staining,real-time polymerase chain reaction(PCR),and Western blotting anlyses.The rat primary cardiomyocytes,breast cancer cell line MDA-MB-23,lung cancer cell line H226,gastric cancer cell line AGS,and bladder cancer cell line 5637 were cultured and divided into control,Adr,Adr+Dex,Dex,and Adr+Dex+NF-κBi groups.CCK-8 and immunofluorescence staining were performed to detect the reactive oxygen species(ROS)contents.Results The myocardial arrangement of the rats in the Adr group was disordered,myocardial cell activity was lower,the mitochondrial membrane potential was lower,ROS production was higher,and NF-κB mRNA and protein contents were sub-stantially lower than those in the control group.The cardiomyocyte morphology was improved,cell activity was higher,mitochondrial mem-brane potential was increased,ROS production decreased,and NF-κB expression significantly increased in the Adr+Dex group compared with those in the control group.The mitochondrial membrane potential in the Adr+Dex+NF-κBi group was lower,and ROS generation was increased compared with the control group.The activity of the tumor cells in the Adr group was lower,and no statistically significant diffe-rences were found compared with that in the Adr+Dex group.Conclusion Treatment with Dex may not affect the chemotherapeutic effects of Adr.Dex administration may increase the myocardial mitochondrial membrane potential and reduce ROS generation by regu-lating NF-κB levels,thereby reducing Adr-induced myocardial damage.关键词
右美托咪定/阿霉素/核因子κB/心肌损伤Key words
dexmedetomidine/adriamycin/nuclear factor κB/myocardial injury分类
医药卫生引用本文复制引用
曹雪峰,赵亮,刘旭东,刘汉成,董天鑫,罗艾静,李艳..右美托咪定通过核因子κB缓解阿霉素诱导的心肌损伤[J].中国医科大学学报,2025,54(4):289-294,6.基金项目
国家自然科学基金(81700310) （81700310）
河北省重点研发计划(22377746D) （22377746D）
河北省中医药管理局科研计划(2024119) （2024119）
河北省泛血管疾病重点实验室开放课题(FXGJBKKFT2403) （FXGJBKKFT2403）
