CAJ | 학술논문

目的探讨2-脱氧葡萄糖 (2-deoxyglucose, 2-DG) 诱导的内质网应激 ( endoplasmic reticulum stress, ERS) 预处理对大鼠脑缺血再灌注后神经细胞凋亡及相关蛋白Bcl-2和Bax表达的影响. 方法 24只SD大鼠随机分为假手术组( SH组)、脑缺血/再灌注组 ( I/R组)、 2-DG诱导的ERS预处理组. 采用TUNEL法检测CA1区凋亡细胞, 免疫组化法检测Bcl-2和Bax蛋白在海马CA1区的表达变化. 结果与I/R组比较, ERS预处理组的神经行为学评分明显降低、凋亡细胞数目亦明显减少 (P<0. 05); Bcl-2蛋白表达细胞数明显增加 (P<0. 01), Bax蛋白表达的细胞数明显减少 (P <0. 01).结论 ERS预处理对脑缺血再灌注损伤具有保护作用, 其机制可能与其影响Bcl-2和Bax蛋白表达有关.
목적 탐토2-탈양포도당 (2-deoxyglucose, 2-DG) 유도적내질망응격 ( endoplasmic reticulum stress, ERS) 예처리대대서뇌결혈재관주후신경세포조망급상관단백Bcl-2화Bax표체적영향. 방법 24지SD대서수궤분위가수술조( SH조)、 뇌결혈/재관주조 ( I/R조)、 2-DG유도적ERS예처리조. 채용TUNEL법검측CA1구조망세포, 면역조화법검측Bcl-2화Bax단백재해마CA1구적표체변화. 결과 여I/R조비교, ERS예처리조적신경행위학평분명현강저、 조망세포수목역명현감소 (P<0. 05); Bcl-2단백표체세포수명현증가 (P<0. 01), Bax단백표체적세포수명현감소 (P <0. 01).결론 ERS예처리대뇌결혈재관주손상구유보호작용, 기궤제가능여기영향Bcl-2화Bax단백표체유관.
Objective To explore the effect of preconditioning the endoplasmic reticulum stress induced by 2-DG on the neural cell apoptosis and the expression of related proteins, Bcl-2 and Bax, in the rats with cerebral ischemic-reperfusion. Method 24 SD rats were divided into 3 groups on average:the sham-operation group ( SH group) , ischemic-reperfusion group ( I/R group) , and en-doplasmic reticulum stress ( induced by 2-DG) preconditioning group ( ERS induced by 2-DG group) . The apoptotic cells in the hipp-ocampal field CA1 were tested with TUNEL, and the Bcl-2 and Bax protein expression changes in the same field were detected with the immunohistochemical method. Result The neurobehavioral scores and the apoptosis cell number significantly decreased in the ERS preconditioning group compared with those in the I/R group (P<0. 05). The cell number of Bcl-2 protein expression significantly in-creased (P<0. 01), while the cells with Bax protein expression significantly decreased (P<0. 01). Conclusion Endoplasmic reticu-lum stress preconditioning provides protection for cerebral ischemic-reperfusion injury by exerting its effect on Bcl-2 and Bax protein expression.