CAJ | 학술논문

目的探讨大鼠创伤性脑损伤急性期高血糖对皮层葡萄糖转运蛋白1(glucose transporter 1,GLUT-1)表达的影响.方法成年雄性SD大鼠180只,随机分成正常对照组,创伤性脑损伤(traumatic brain injury,TBI)组,胰岛素治疗组,分别测定各组伤前伤后血糖值,采用RT-PCR法和Western-blot法测定各组伤侧及健侧皮层GLUT-1基因和蛋白的表达,应用TUNEL法测定各组伤侧及健侧皮层凋亡细胞数.结果 TBI组伤后血糖明显升高,伤侧皮层GLUT-1表达明显减少,凋亡细胞数明显增多;胰岛素治疗组血糖变化不明显(P＞0.05),伤后12 h,24 h,48 h,72 h GLUT-1表达明显多于TBI组(P均＜0.01),凋亡细胞数明显少于TBI组(P均＜0.01);各组健侧皮层GLUT-1表达和凋亡细胞数未见明显变化(P＞0.05).结论 TBI急性期高血糖可增加伤后脑细胞凋亡,其机制可能与TBI急性期高血糖下调GLUT-1表达有关.
목적 탐토대서창상성뇌손상급성기고혈당대피층포도당전운단백1(glucose transporter 1,GLUT-1)표체적영향.방법 성년웅성SD대서180지,수궤분성정상대조조,창상성뇌손상(traumatic brain injury,TBI)조,이도소치료조,분별측정각조상전상후혈당치,채용RT-PCR법화Western-blot법측정각조상측급건측피층GLUT-1기인화단백적표체,응용TUNEL법측정각조상측급건측피층조망세포수.결과 TBI조상후혈당명현승고,상측피층GLUT-1표체명현감소,조망세포수명현증다;이도소치료조혈당변화불명현(P＞0.05),상후12 h,24 h,48 h,72 h GLUT-1표체명현다우TBI조(P균＜0.01),조망세포수명현소우TBI조(P균＜0.01);각조건측피층GLUT-1표체화조망세포수미견명현변화(P＞0.05).결론 TBI급성기고혈당가증가상후뇌세포조망,기궤제가능여TBI급성기고혈당하조GLUT-1표체유관.
Objective Aim to explore the effect of hyperglycemia on the expression of glucose transporter 1 (GLUT-1)in rats at the acute phase of traumatic brain injury.Methods Adult male SD rats were randomly divided into 3 groups: normal control group, traumatic brain injury group and insulin treated group.The blood glucose concentration of the rats was measured before and after injury.The expression of GLUT-1 gene and protein in the injured and uninjured cortex was detected by reverse transcription polymerase chain reaction (RT-PCR) and western-blot.The apoptosis in the injured and uninjured cortex were detected by TUNEL staining.Results The blood glucose concentration increased markedly in traumatic brain injury group.The expression of GLUT-1 gene and protein in the injured cortex decreased in both the traumatic brain injury group and the insulin treated group.In contrast, the expression of GLUT-1 gene and protein significantly increased at 12 h, 24 h, 48 h, 72 h after injury in the insulin treated group compared with control(P＜0.01).The number of apoptotic cells in the insulin treated group were significantly larger than that in the traumatic brain injury group at each time point(P＜0.01).However, The number of apoptotic cell death remained unchange in the uninjured cortex in each group(P＞0.05).Conclusions The hyperglycemia after traumatic brain injury may increase the apoptotic cells in the injured brain through decreasing the expression of GLUT-1.