The Protection Effect Of Triiodothyronine On The Apoptosis Of Immature Cadiocytes While Given Ischemical Reperfusion Injury

Objective: Low thyroxin has been associated with short-term mortality of patient in intensive care and long-term motality of patient with heart disease. This research would administer triiodothyronine to isolated cultured cadiocytes of neonate rat shortly before anoxia-reoxygenation,and explore whether the apoptosis of immature cadiocyte would reduce or not while given ischemical reperfusion injury.Further more,We would explore the relationship between the effects of T3 and Bcl-2/Bax expression, and also the KATP channel.Methods: The cadiocytes of neonate rat were culrured in vitro,The ischemical reperfusion injury of cadiocytes were induced by anoxia-reoxygenation.T3 and glibenclamide was administered before anoxia-reoxygenation at a concentration of 1ng/ml, Bcl-2 mRNA and Bax mRNA were detected by PCR,and the apoptosis of cadiocytes were detected by TUNEL.Results: The bcl-2 were down-regulation and Bax were up-regulation while given T3 shortly before anoxia-reoxygenation.At the same time, the apoptosis of cadiocytes were reduced.This protection could be blocked by Glibenclamide,which is a KATP channel blocker.Conclusion:Give Triiodothyronine before anoxia-reoxygenation would enhance the ablity of immature cadiocytes against ischemical reperfusion injury,and could reduce the apoptosis of cadiocytes.This effects were associated with the expression of Bcl-2 and Bax ,and this effects could be blocked by Glibenclamide,which is a KATP channel blocker.