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Upregulated Hsp27 Expression in the Cardioprotection Induced by Acute Stress and Oxytocin in Ischemic Reperfused Hearts of the Rat

並列摘要


In view of the cardloprotective effect of oxytocin (OT) released in response to stress, the aim of this stud y was to evaluate the role of heat shock proteins Hsps 70, 27 and 20 in stress-induced cardioprotection in isolated, perfused rat hearts. Rats were divided in two main groups: unstressed and stressed rats, and all of them were subjected to i.c.v, infusion of vehicle or drugs: unstressed rats (control: vehicle, OT (100 ng /5 μl), atosiban (ATO; 4.3 μg/5 μl) as OT antagonist, ATO+OT I, and stressed rats 1St: stress, OT+St, ATO+Stl. After anesthesia, hearts were isolated and subjected to 30 min regional ischemia and 60 min subsequent reperfusion (TR), Acute stress protocol included swimming for 10 min before anesthesia. Malondialdehyd e in coronary effluent was measured and the expression of Hsp 70, 27 and 20 was measured in myocardium using re al-time reverse transcriptase polymerase chain reaction (RT-PCR). The ma londialdehyde levels, which decreased in the St and OT groups, increased by the administration of atosiban as an OT antagonist. The expression of Hsp27 increased 4 to 5 folds by stress induction and i.c.v. infusion of OT. Central administration of atosiban prior to both stress and OT decreased Hsp27 mRNA levels. These finding s suggest that endogenous OT may participate in stress-induced cardioprotection via Hsp27 over-expression as an early response.

並列關鍵字

heart heat shock proteins ischemia oxytocin receptor reperfusion stress

參考文獻


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