Cardioprotective Effects of Transfusion of Late-Phase Preconditioned Plasma May Be Induced by Activating the Reperfusion Injury Salvage Kinase Pathway but Not the Survivor Activating Factor Enhancement Pathway in Rats.
Cardioprotective Effects of Transfusion of Late-Phase Preconditioned Plasma May Be Induced by Activating the Reperfusion Injury Salvage Kinase Pathway but Not the Survivor Activating Factor Enhancement Pathway in Rats.
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输注后期预处理血浆的心脏保护作用可能是通过激活大鼠再灌注损伤挽救激酶途径而非幸存者激活因子增强途径诱导的
DOI：
10.1155/2017/8526561
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发表时间：
2017
影响因子：
--
通讯作者：
Jin SQ
中科院分区：
文献类型：
--
作者：
Zhao Y;Zheng ZN;Pi YN;Liang X;Jin SQ
本实验室先前的研究表明，在远程缺血预适应（RIPC）晚期收集的血浆回输可减少心肌梗死范围。在这里，我们测试是否再灌注损伤补救激酶（RISK）和幸存者激活因子增强（SAFE）途径参与转移保护。在两部分研究中，供体大鼠（n = 3）在RIPC（预处理血浆）或对照（非预处理血浆）后48小时捐献血浆。正常（第1部分）或缺血（第2部分）心肌收集受体（n = 6）24小时后，接受生理盐水，非预处理的血浆，和预处理的血浆或进一步遭受缺血再灌注。Western blot检测正常和缺血心肌（中央区和交界区）中STAT 3、Akt和Erk 1/2的磷酸化水平。在正常心肌，预处理血浆增加Akt和Erk 1/2磷酸化显着相比，nonpreconditioned血浆和生理盐水;没有STAT 3磷酸化检测。在缺血性心肌，预处理血浆增加Akt和Erk 1/2磷酸化显着在中央和边缘地区相比，其他液体，STAT 3磷酸化组间无显着差异。在RIPC晚期采集的预处理血浆输注可激活RISK通路，但不激活SAFE通路，提示RISK通路可能参与保护的传递。
A previous study in our laboratory demonstrated that transfusion of plasma collected at the late phase of remote ischemic preconditioning (RIPC) could reduce myocardial infarct size. Here, we tested whether the reperfusion injury salvage kinase (RISK) and survivor activating factor enhancement (SAFE) pathways are involved in transferring protection. In a two-part study, donor rats (n = 3) donated plasma 48 hours after RIPC (preconditioned plasma) or control (nonpreconditioned plasma). Normal (part 1) or ischemic (part 2) myocardia were collected from recipients (n = 6) 24 hours after receiving normal saline, nonpreconditioned plasma, and preconditioned plasma or after further suffering ischemia reperfusion. Western blot was performed to analyze STAT3, Akt, and Erk1/2 phosphorylation in normal and ischemic myocardium (central area and border area). In normal myocardia, preconditioned plasma increased Akt and Erk1/2 phosphorylation significantly compared to nonpreconditioned plasma and normal saline; no STAT3 phosphorylation was detected. In ischemic myocardia, preconditioned plasma increased Akt and Erk1/2 phosphorylation significantly in both central and border areas compared to other fluids; no significant difference in STAT3 phosphorylation occurred among groups. Transfusion of preconditioned plasma collected at the late phase of RIPC could activate the RISK but not SAFE pathway, suggesting that RISK pathway may be involved in transferring protection.
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影响因子：
10.8
作者：
Suleman, Naushaad;Somers, Sarin;Lecour, Sandrine C.
通讯作者：
Lecour, Sandrine C.
影响因子：
3
作者：
Lai, Chang-Chi;Tang, Chia-Yu;Huang, Cheng-Hsiung
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Huang, Cheng-Hsiung
影响因子：
6
作者：
Shimizu, Mikiko;Tropak, Michael;Redington, Andrew N.
通讯作者：
Redington, Andrew N.
影响因子：
10.7
作者：
Sivaraman V;Pickard JM;Hausenloy DJ
通讯作者：
Hausenloy DJ
影响因子：
37.8
作者：
Lecour, S;Suleman, N;Opie, LH
通讯作者：
Opie, LH