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首页|期刊导航|中国药理学通报|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

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

李启航 朱华 马紫微 张曼茹 于华青 葛凤琴 宋雨晨 郭丹丹 赵静 杭鹏洲

中国药理学通报2024,Vol.40Issue(4):716-722,7.
中国药理学通报2024,Vol.40Issue(4):716-722,7.DOI:10.12360/CPB202306002

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

李启航 1朱华 2马紫微 3张曼茹 3于华青 3葛凤琴 1宋雨晨 1郭丹丹 1赵静 2杭鹏洲2

作者信息

  • 1. 扬州大学临床医学院,苏北人民医院,江苏扬州 225001||扬州大学医学院,江苏扬州 225009
  • 2. 扬州大学临床医学院,苏北人民医院,江苏扬州 225001
  • 3. 扬州大学临床医学院,苏北人民医院,江苏扬州 225001||大连医科大学,辽宁大连 116000
  • 折叠

摘要

Abstract

Aim To investigate the effects of 7,8-di-hydroxyflavone(7,8-DHF)on LPS-induced cardio-myocyte injury and the underlying mechanisms.Meth-ods 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.Mi-tosox fluorescent probe was used to detect the mito-chondrial oxidative stress in cardiomyocytes.Western blot was employed to examine the expression of key proteins including Akt,nuclear factor-KB(NF-κB)p65,and signal transducer and activator of transcrip-tion 3(STAT3).Results 7,8-DHF increased cell viability and inhibited cell death and mitochondrial oxi-dative 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 in-jury,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

Key words

cardiomyocyte/7,8-DHF/LPS/oxida-tive stress/NFκB/STAT3

分类

医药卫生

引用本文复制引用

李启航,朱华,马紫微,张曼茹,于华青,葛凤琴,宋雨晨,郭丹丹,赵静,杭鹏洲..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[J].中国药理学通报,2024,40(4):716-722,7.

基金项目

国家自然科学基金资助项目(No 81870191) (No 81870191)

中国药理学通报

OA北大核心CSTPCD

1001-1978

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