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Heat shock protein (HSP) 70 plays a critical role in protecting the heart from various stressor-induced cell injuries; the mechanism remains to be further understood. The present study aims to elucidate the effect of a probiotics-derived protein, LGG-derived protein p75 (LGP), in alleviating the ischemia/reperfusion (I/R)-induced heart injury. We treated rats with the I/R with or without preadministration with LGP. The levels of HSP70 and carboxy terminus of HSP70-interacting protein (CHIP) in the heart tissue were assessed by enzyme-linked immunosorbent assay (ELISA) and Western blotting. The effect of CHIP on suppression of HSP70 and the effect of LGP on suppression of CHIP were investigated with an I/R rat model and a cell culture model. The results showed that I/R-induced infarction in the heart could be alleviated by pretreatment with LGP. HSP70 was detected in naïve rat heart tissue extracts. I/R treatment significantly suppressed the level of HSP70 and increased the levels of CHIP in the heart. A complex of CHIP/HSP70 was detected in heart tissue extracts. The addition of recombinant CHIP to culture inhibited HSP70 in heart cells. LGP was bound CHIP in heart cells and prevented the CHIP from binding HSP70. In summary, I/R can suppress HSP70 and increase CHIP in heart cells. CHIP can suppress HSP70 that can be prevented by pretreatment with LGP. The results imply that CHIP may be a potential target in the prevention of I/R-induced heart cell injury.

Objective: Adenosine pretreatment reduces injury caused by ischemia-reperfusion. To investigate the hypothesis that adenosine pretreatment would modulate injury induced by cardiopulmonary bypass (CPB) and myocardial ischemia/reperfusion, we conducted a randomized controlledtrial ontheeffects of adenosinepretreatment inchildrenundergoingsurgery to repaircongenitalheart defects.Methods:Children undergoing surgery to repair congenital heart defects were randomized to adenosine pretreatment or control treatment. Adenosine pretreatment was performed by infusing a total of 2.45 mg kg 1 of adenosine over 10 min. Serum troponin I was measured pre- and postoperatively. Multiple clinical parameters, including postoperative use of inotropic medicine and duration in the intensive care unit (ICU),wererecorded.Results:Atotalof82patientswereenrolledinthestudy.Therewere42controlpatientsand40patientsintheadenosine pretreatment group. The mean age and weight of the two groups were notsignificantly different, nor were cardiopulmonary bypass and crossclamp times. There were no deaths and severe complications in both groups. The adenosine pretreatment protocol caused significant hypotension but had no significant effect on heart rate. One patient had severe tachycardia shortly after the adenosine pretreatment protocol was completed, and adenosine infusion was continued until CPB was started. Postoperative levels of serum troponin I were greater in the controlpatientsthaninthe adenosinepretreatmentgroup,indicating thatthecontrolgroupsufferedgreatermyocardialinjury.Controlgroup patients required more postoperative inotropic agents than those in the adenosine pretreatment group at 0, 1, and 3 h, indicating that the adenosinepretreatment grouphadabettercardiac function.The adenosine pretreatment group also required significantly less time in the ICU than the control group (3.2 1.2 days vs 3.9 1.2 days, p = 0.013). Conclusions: This study demonstrates that adenosine pretreatment is protective of the myocardium during open-heart surgery in pediatric patients. # 2011 European Association for Cardio-Thoracic Surgery. Published by Elsevier B.V. All rights reserved.