ty -jour a2 -valacchi，giuseppe au -yeh，chi -hsiao au -chen，tzu -ping au -wang，wang，yao -chang au -lin，lin，yu -min au -fang -fang，shu -wen py -shu -wen py -2010 da -2011/2011/2011/2011/2011/2011/2011/01/23 TI - AMP-Activated Protein Kinase Activation during Cardioplegia-Induced Hypoxia/Reoxygenation Injury Attenuates Cardiomyocytic Apoptosis via Reduction of Endoplasmic Reticulum Stress SP - 130636 VL - 2010 AB - Cardioplegic-induced H/R injury results in cardiomyocytic apoptosis.已显示AMPK可减少ER应力和展开的蛋白质反应（UPR）。在心脏地质诱导的H/R损伤后，AMPK激活是否可以减弱心肌细胞凋亡是尚不清楚的。通过在低氧室中与间歇性冷心脏双毛干性溶液在低氧室中孵育，以20分钟的间隔将心肌细胞暴露于模拟缺血，随后在常氧环境中恢复活氧。在H/R损伤前2天给出了各种剂量的AMPK激活剂（AICAR或二甲双胍）。重氧后收获心肌细胞以进行后续检查。对于两个AMPK激活剂，ER应激和UPR的抗凋亡基因，随后的促凋亡蛋白的产生被衰减，并升高了抗凋亡蛋白。通过AMPK激活，ER应激的凋亡效应子的活性也降低。此外，TUNEL染色表明，AMPK激活显着降低了心脏双痛引起的H/R损伤后凋亡心肌细胞的百分比。 Our results revealed that AMPK activation during cardioplegia-induced H/R injury attenuates cardiomyocytic apoptosis, via enhancement of antiapoptotic and reduction of proapoptotic responses, resulting from lessening ER stress and the UPR. AMPK activation may serve as a future pharmacological target to reduce H/R injury in the clinical setting. SN - 0962-9351 UR - https://doi.org/10.1155/2010/130636 DO - 10.1155/2010/130636 JF - Mediators of Inflammation PB - Hindawi Publishing Corporation KW - ER -