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典型文献
Didymin attenuates doxorubicin-induced cardiotoxicity by inhibiting oxidative stress
文献摘要:
Objective:This study was designed to investigate the protective effects of didymin(Did)on doxorubicin(DOX)-induced cardiotoxicity.Methods:After pretreatment with Did(2,4,8 mg/kg intraperitoneal i.p.)for 7 d,the male C57 mice were injected with single dose of DOX(20 mg/kg i.p.).The cardioprotective effect of Did was observed on the 7th day after DOX treatment.Results:DOX delayed body growth and caused cardiac tissue injury,oxidative stress,and mitochondrial dysfunction.Similar experiments in H9C2 cardiomyocytes showed that DOX reduced cell viability,increased generation of reactive oxygen species(ROS)and fragmentation of DNA,decreased mitochon-drial membrane potential,and induced cardiomyocyte apoptosis.However,all of these adverse effects were suppressed by Did pretreatment.Did increased protein expression of glutamate-L-cysteine ligase catalytic subunit(GCL),heme oxygenase 1(HO-1),and nuclear factor erythroid 2-related factor 2(Nrf2).Besides,Did also induced activation of PI3K/AKT.Conclusion:These findings indicated Did prevented DOX-induced cardiac injury and apoptosis via acti-vating PI3K/AKT/Nrf2 signaling pathway.
文献关键词:
作者姓名:
Rongchang Chen;Guibo Sun;Lijiao Xu;Xu Zhang;Wenying Zeng;Xiaobo Sun
作者机构:
Institute of Medicinal Plant Development,Peking Union Medical College and Chinese Academy of Medical Sciences,Beijing 100193,China;Department of Comprehensive Medicine,Xiyuan Hospital,China Academy of Chinese Medical Sciences,Beijing 100091,China
引用格式:
[1]Rongchang Chen;Guibo Sun;Lijiao Xu;Xu Zhang;Wenying Zeng;Xiaobo Sun-.Didymin attenuates doxorubicin-induced cardiotoxicity by inhibiting oxidative stress)[J].中草药(英文版),2022(01):70-78
A类:
Didymin,didymin,vating
B类:
attenuates,doxorubicin,induced,cardiotoxicity,by,inhibiting,oxidative,stress,Objective,This,study,was,designed,investigate,effects,DOX,Methods,After,pretreatment,intraperitoneal,male,C57,mice,were,injected,single,dose,cardioprotective,observed,7th,day,after,Results,delayed,body,growth,caused,cardiac,tissue,injury,mitochondrial,dysfunction,Similar,experiments,H9C2,cardiomyocytes,showed,that,reduced,cell,viability,increased,generation,reactive,species,ROS,fragmentation,decreased,membrane,potential,apoptosis,However,all,these,adverse,suppressed,protein,expression,glutamate,cysteine,ligase,catalytic,subunit,GCL,heme,oxygenase,HO,nuclear,erythroid,related,Nrf2,Besides,also,activation,PI3K,AKT,Conclusion,These,findings,indicated,prevented,signaling,pathway
AB值:
0.57962
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