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桃叶珊瑚苷通过 ERβ途径抑制 TNF-α诱导的心脏祖细胞凋亡

李春晓 李慧影 王虹 陈璐 邱丽珍 耿潇 尤星宇

中国药理学通报2016,Vol.32Issue(8):1068-1074,7.
中国药理学通报2016,Vol.32Issue(8):1068-1074,7.DOI:10.3969/j.issn.1001-1978.2016.08.008

桃叶珊瑚苷通过 ERβ途径抑制 TNF-α诱导的心脏祖细胞凋亡

Aucubin inhibited apoptosis of mouse cardiac progenitor cells induced by TNF-αthrough ERβpathway

李春晓 1李慧影 1王虹 1陈璐 1邱丽珍 1耿潇 1尤星宇1

作者信息

  • 1. 天津中医药大学,天津市现代中药重点实验室-省部共建国家重点实验培育基地,天津市中药药理学重点实验室,方剂学教育部重点实验室,天津 300193
  • 折叠

摘要

Abstract

Aim Aucubin(AU) is one of the effective ingredients of eucommia , plantain , rehmannia and oth-er herbs.Modern pharmacological studies have shown that AU has protective effects on immunity , cardiovas-cular and nervous system , but its mechanism is un-clear .Previous studies have confirmed that AU can ac-tivate estrogen receptor , suggesting that AU may play a role in cardiovascular protection through estrogen signa-ling pathway .In recent years , more and more evidence showed that cardiac progenitor cells ( CPCs ) play an important role in the repair of myocardial ischemic in-jury.Methods To further elucidate the mechanism , our study used mouse CPCs as cell model and elucida-ted the effect of AU on CPCs apoptosis induced by tumor necrosis factor alpha ( TNF-α) and its mecha-nism by IncuCyte live cell imaging , TUNEL staining , Western blot and quantitative PCR . Results AU could reduce TNF-α-induced apoptosis of CPCs , de-crease the expression of caspase-3 and up-regulate Bcl-2/Bax levels.Estrogen receptor beta ( ERβ) antagonist could block the anti-apoptotic effect of AU , and AU treatment was able to increase the expression of ERβ. Conclusion AU could inhibit the apoptosis of CPCs induced by TNF-α, and its mechanism is the activation of ERβpathway .

关键词

桃叶珊瑚苷/心脏祖细胞/雌激素受体β/肿瘤坏死因子-α/细胞凋亡/组织损伤修复

Key words

aucubin/cardiac progenitor cells/estro-gen receptor β/tumor necrosis factor-α/cell apopto-sis/tissue injury repair

分类

医药卫生

引用本文复制引用

李春晓,李慧影,王虹,陈璐,邱丽珍,耿潇,尤星宇..桃叶珊瑚苷通过 ERβ途径抑制 TNF-α诱导的心脏祖细胞凋亡[J].中国药理学通报,2016,32(8):1068-1074,7.

基金项目

新世纪优秀人才支持计划( No NCET-13-0935);国家自然科学基金资助项目( No 81173592);国家国际科技合作专项(No 2015DFA30430);长江学者和创新团队发展计划资助项目 ()

中国药理学通报

OA北大核心CSCDCSTPCD

1001-1978

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