μ-CALPAIN REGULATE CARDIOMYOCYTES APOPTOSIS VIA APOPTOSIS INDUCING FACTOR AND BID IN RAT HEART ISCHAEMIA/REPERFUSION INJURY

Autor:	Song Zhao-Feng, Chen Dong-Yu, Du Bo, Wang Li-Zhen, Wang Fan, Qi Xin-Yan, Zhou Qing-Hua
Rok vydání:	2012
Předmět:	Cardiac function curve biology Ischaemia-reperfusion injury business.industry Calpain Rat heart Pharmacology Pathogenesis Toxicology Apoptosis biology.protein Apoptosis-inducing factor Medicine Cardiology and Cardiovascular Medicine business
Zdroj:	Heart. 98:E50.1-E50
ISSN:	1468-201X 1355-6037
DOI:	10.1136/heartjnl-2012-302920a.120
Popis:	Objectives Heart I/R may exacerbate myocardial injury by the release of massive of reactive oxygen and nitrogen species. Calpain has been proposed to play a role in the pathogenesis of heart I/R injury. However, the underlying mechanisms are still not thoroughly understood. Here we investigated the effect of μ-Calpain on heart I/R injury and elucidated the underlying mechanisms. Methods Studies were performed with I/R rats9 hearts. MDL-281703, a μ-Calpain inhibitor, was used to inhibit the activate of μ-Calpain. The cardiac function and cells apoptosis were detected. The activation of μ-Calpain, Bid and Apoptosis-inducing factor (AIF) were evaluated during the I/R protocol. Results During the I/R protocol, the 76 kDa size of fragment, which was active fragment of μ-Calpain, significantly increased. In the same time, the expression of AIF in nuclear and Bid also increased. Administration of MDL-281703 decreased cells apoptosis from 36±3.9% to 25±7.1% p Conclusions Our results suggested that μ-Calpain played a role of cells apoptosis in rats heart I/R injury. In this process, μ-Calpain regulate cardiomyocytes apoptosis via both caspase-dependent pathway (Bid) and non-caspase dependent pathway (AIF).
Databáze:	OpenAIRE
Externí odkaz:	https://explore.openaire.eu/search/publication?articleId=doi_________::f3d391ed9ad8d9fbdf71051f7f099785 https://doi.org/10.1136/heartjnl-2012-302920a.120 Zobrazit plný text záznamu