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Erschienen in: Cardiovascular Toxicology 1/2011

01.03.2011

Protective Effect of FK506 on Myocardial Ischemia/Reperfusion Injury by Suppression of CaN and ASK1 Signaling Circuitry

verfasst von: Xing Feng, Jing Li, Jinyu Liu, Minghua Jin, Xiaomei Liu, Haiying Du, Long Zhang, Zhiwei Sun, Xiaoguang Li

Erschienen in: Cardiovascular Toxicology | Ausgabe 1/2011

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Abstract

We investigated protective effect of FK506 on rat hearts subjected to ischemia/reperfusion (I/R) injury by regulating CaN and ASK1. Wistar rats were divided into four groups: Ischemia/reperfusion group (I/R), FK506 + Ischemia/reperfusion group (FK506-I/R), sham group, and FK506 + sham group (FK506-sham). Ischemia/reperfusion was achieved by occluding left coronary artery for 30 min and subsequently reperfusing for 120 min. FK506 was administered 15 min before ischemia. Rats in sham group and FK506-sham group were operated only by placing a ligature around the coronary artery, and the blood supply was not blocked. I/R group showed a rapid increase in TUNEL-positive cells and high risks of histopathological changes in damaged cardiac tissues. FK506 reduced the infarct size and inhibited the activation of CaN enzyme in FK506-I/R group. Increase in Bcl-2/Bax ratio in FK506-IR group indicated that FK506 protected myocardium from apoptosis induced by IR. The activity of CaN and ASK1 protein level decreased significantly after I/R injury in FK506-treated I/R heart. FK506 suppresses the activation of CaN and ASK1 through CaN-mediated apoptosis pathway, and ASK1 negatively regulates CaN activity. Suppression of CaN and ASK1 signaling circuitry are involved in protective effect of FK506 on rat myocardium I/R injury.
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Metadaten
Titel
Protective Effect of FK506 on Myocardial Ischemia/Reperfusion Injury by Suppression of CaN and ASK1 Signaling Circuitry
verfasst von
Xing Feng
Jing Li
Jinyu Liu
Minghua Jin
Xiaomei Liu
Haiying Du
Long Zhang
Zhiwei Sun
Xiaoguang Li
Publikationsdatum
01.03.2011
Verlag
Humana Press Inc
Erschienen in
Cardiovascular Toxicology / Ausgabe 1/2011
Print ISSN: 1530-7905
Elektronische ISSN: 1559-0259
DOI
https://doi.org/10.1007/s12012-010-9095-6

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