7,8-二羟基黄酮对脂多糖诱导心肌细胞损伤的保护作用及机制研究  

The protective effect of 7,8-dihydroxyflavone on lipopolysaccharide-induced cardiomyocyte injury and its mechanism

作　　者：李启航 马紫微 张曼茹 于华青 葛凤琴 宋雨晨 郭丹丹 赵静 杭鹏洲 朱华[1] LI Qi-hang;MA Zi-wei;ZHANG Man-ru;YU Hua-qing;GE Feng-qin;SONG Yu-chen;GUO Dan-dan;ZHAO Jing;HANG Peng-zhou;ZHU Hua(Clinical Medical College,Yangzhou University,Northern Jiangsu People′s Hospital,Yangzhou Jinagsu 225001,China;Medical College,Yangzhou University,Yangzhou Jiangsu 225009,China;Dalian Medical University,Dalian Liaoning 116000,China)

机构地区：[1]扬州大学临床医学院,苏北人民医院,江苏扬州225001 [2]扬州大学医学院,江苏扬州225009 [3]大连医科大学,辽宁大连116000

出　　处：《中国药理学通报》2024年第4期716-722,共7页Chinese Pharmacological Bulletin

基　　金：国家自然科学基金资助项目(No 81870191)。

摘　　要：目的研究7,8-二羟基黄酮(7,8-dihydroxyflavone,7,8-DHF)在脂多糖(lipopolysaccharide,LPS)诱导心肌细胞损伤中的作用及机制。方法传代培养H9c2心肌细胞系,随机分为对照组(Ctrl)、LPS组、LPS+7,8-DHF组和7,8-DHF单独处理组,给药24 h后观察细胞形态,分别采用MTT法检测细胞活力、Live/Dead染色检测细胞活死比例、Mitosox染色检测细胞线粒体氧化应激水平,Western blot技术检测Akt、核因子κB(NF-κB)p65、信号传导和转录激活因子3(signal transducer and activator of transcription 3,STAT3)等蛋白表达水平。结果7,8-DHF增加LPS诱导的心肌细胞活力,减少氧化应激水平和细胞死亡。7,8-DHF激活LPS诱导的心肌细胞Akt信号,抑制STAT3磷酸化水平和NF-κB p65蛋白表达。结论7,8-DHF可能通过激活Akt、抑制磷酸化STAT3和NF-κB p65信号分子减轻LPS诱导的心肌细胞损伤。Aim To investigate the effects of 7,8-dihydroxyflavone(7,8-DHF)on LPS-induced cardiomyocyte injury and the underlying mechanisms.Methods H9c2 cardiomyocyte cell line was subcultured and randomly divided into control group(Ctrl),LPS group,LPS+7,8-DHF group,and 7,8-DHF-alone group.Cell morphology was observed after treatment for 24 h.MTT assay and Live/Dead staining were used to determine the cell viability and the death ratio.Mitosox fluorescent probe was used to detect the mitochondrial oxidative stress in cardiomyocytes.Western blot was employed to examine the expression of key proteins including Akt,nuclear factor-κB(NF-κB)p65,and signal transducer and activator of transcription 3(STAT3).Results 7,8-DHF increased cell viability and inhibited cell death and mitochondrial oxidative stress in LPS-induced cardiomyocytes.7,8-DHF activated Akt,whereas inhibited protein expression of phosphorylated STAT3 and NF-κB p65.Conclusions 7,8-DHF attenuates LPS-induced cardiomyocyte injury,which is associated with the activation of Akt and the inhibition of STAT3 phosphorylation and NF-κB p65 signals.

关 键 词：心肌细胞 7 8-二羟基黄酮 脂多糖 氧化应激 核因子ΚB 信号转导和转录激活因子3 

分 类 号：R-332[医药卫生] R329.24R329.411R349.1R631R977.6