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The PI3K/Akt pathway mediates the protection of SO2 preconditioning against myocardial ischemia/reperfusion injury in rats
Zhao, Man-man1; Yang, Jin-yan1; Wang, Xin-bao1; Tang, Chao-shu2,3; Du, Jun-bao1,2; Jin, Hong-fang1
关键词sulfur dioxide ischemia/reperfusion heart infarct preconditioning LDH creatine kinase caspase-3 caspase-9 PI3K/Akt pathway LY294002
刊名ACTA PHARMACOLOGICA SINICA
2013-04-01
DOI10.1038/aps.2012.204
34期:4页:501-506
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Chemistry, Multidisciplinary ; Pharmacology & Pharmacy
资助者Major Basic Research Program of China ; National Natural Science Foundation of China ; Major Basic Research Program of China ; National Natural Science Foundation of China
研究领域[WOS]Chemistry ; Pharmacology & Pharmacy
关键词[WOS]PERMEABILITY TRANSITION PORE ; BISULFITE SULFUR-DIOXIDE ; ISCHEMIA-REPERFUSION ; ACTIVATION ; HEART ; CARDIOPROTECTION ; METABOLISM ; INFARCTION ; STRESS ; KINASE
英文摘要

Aim: To explore the mechanisms underlying the protection by SO2 preconditioning against rat myocardial ischemia/reperfusion (I/R) injury.

Methods: Male Wistar rats underwent 30-min left coronary artery ligation followed by 120-min reperfusion. An SO2 donor (1 mu mol/kg) was intravenously injected 10 min before the ischemia, while LY294002 (0.3 mg/kg) was intravenously injected 30 min before the ischemia. Plasma activities of LDH and CK were measured with an automatic enzyme analyzer. Myocardial infarct size was detected using Evans-TTC method. The activities of caspase-3 and -9 in myocardium were assayed using a commercial kit, and the levels of p-Akt, Akt, PI3K and p-PI3K were examined with Western blotting.

Results: Pretreatment with SO2 significantly reduced the myocardial infarct size and plasma LDH and CK activities, as well as myocardial caspase-3 and -9 activities in the rats. Furthermore, the pretreatment significantly increased the expression levels of myocardial p-Akt and p-PI3K p85. Administration of the PI3K inhibitor LY294002 blocked all the effects induced by SO2 pretreatment.

Conclusion: The results suggest that the PI3K/Akt pathway mediates the protective effects of SO2 preconditioning against myocardial I/R injury in rats.

语种英语
所属项目编号2012CB517806 ; 2011CB503904 ; 81121061 ; 81070111 ; 31130030 ; 81070212
资助者Major Basic Research Program of China ; National Natural Science Foundation of China ; Major Basic Research Program of China ; National Natural Science Foundation of China
WOS记录号WOS:000317106600008
引用统计
被引频次:20[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/65633
专题北京大学第一临床医学院_儿科
作者单位1.Minist Educ, Key Lab Mol Cardiol, Beijing 100191, Peoples R China
2.Peking Univ, Hosp 1, Dept Pediat, Beijing 100034, Peoples R China
3.Peking Univ, Dept Physiol & Pathophysiol, Hlth Sci Ctr, Beijing 100191, Peoples R China
推荐引用方式
GB/T 7714
Zhao, Man-man,Yang, Jin-yan,Wang, Xin-bao,et al. The PI3K/Akt pathway mediates the protection of SO2 preconditioning against myocardial ischemia/reperfusion injury in rats[J]. ACTA PHARMACOLOGICA SINICA,2013,34(4):501-506.
APA Zhao, Man-man,Yang, Jin-yan,Wang, Xin-bao,Tang, Chao-shu,Du, Jun-bao,&Jin, Hong-fang.(2013).The PI3K/Akt pathway mediates the protection of SO2 preconditioning against myocardial ischemia/reperfusion injury in rats.ACTA PHARMACOLOGICA SINICA,34(4),501-506.
MLA Zhao, Man-man,et al."The PI3K/Akt pathway mediates the protection of SO2 preconditioning against myocardial ischemia/reperfusion injury in rats".ACTA PHARMACOLOGICA SINICA 34.4(2013):501-506.
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