中文摘要：

目的：研究缺氧预处理（hypoxic preconditioning，HPC）对内质网应激（endoplasmic reticulum stress，ERS）所致的心肌微血管内皮细胞（microvascutar endothelial cells，MVECs）损伤的影响。方法：以毒胡萝卜素（thap-sigargin，TG）诱导大鼠心肌MVECs ERS，以乳酸脱氢酶（1actate dehydrogenase，LDH）漏出和细胞凋亡率检测细胞损伤，phalloidin—FITC荧光染色和内质网染色分别观察细胞骨架和细胞内质网形态变化，双向电泳一质谱技术检测TG作用后内皮细胞蛋白质谱表达变化，Western blotting技术检测ERS相关的分子表达。结果：TG剂量依赖性诱导MVECs LDH漏出和细胞凋亡，并出现内质网应激分子钙网蛋白（calreticulin，CRT）和葡萄糖调节蛋白78（slu-cose．regulated protein78，GRP78）表达上调；HPC减轻TG诱导的MVECs损伤，并可以抑制TG诱导的ERS相关分子的表达上调。结论：HPC减轻内质网应激所致的大鼠心肌MVECs损伤。

英文摘要：

AIM： To investigate the effect of hypoxic preconditioning （HPC） on endoplasmic reticulum stress （ERS）-induced injury in cultured microvascular endothelial cells （MVECs） from rat hearts. METHODS： MVECs injury was induced by an ERS inductor thapsigargin （TG）. Lactate dehydrogenase （LDH） leakage and apoptotic rate were detec-ted to evaluate the injury of MVECs. Cytoskeleton and endoplasmic reticulum （ER） in MVECs were observed by phalloi-din-FITC fluorescence staining and ER staining, respectively. Two-dimensional electrophoresis and mass spectrometry （MS） were used to identify proteomic profile in MVECs treated with TG. Western blotting was used to detect the expression of ERS markers, calreticulin （CRT） and glucose-regulated protein 78 （GRF78）. RESULTS： TG induced the increase in LDH activity in medium and the apoptosis of MVECs in a dose-dependent manner. TG treatment up-regulated the expres-sion of CRT and GRP78, while HPC attenuated the ERS-induced injury and the up-regulation of ERS markers in MVECs. CONCLUSION： HPC protects MVECs from ERS-induced injury.