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目的探讨谷氨酸转运体(EAAT)在糖尿病脑损伤时表达情况及作用机制。方法 Wistar大鼠28只,随机分成2组(每组14只):对照组(常规饲料喂养)、模型组(高糖高脂饲料喂养+STZ注射诱导胰岛素抵抗),均自由进食进水,12h光照周期。饲养1个月后,测定血糖。6个月后以RT-PCR检测大鼠脑皮质EAAT-1、EAAT-2、EAAT-3的mRNA表达情况。结果糖尿病模型组血糖[(20.016±1.984)mmol/L]明显高于正常值(P<0.01)及对照组[(3.82±0.123)mmol/L,P<0.01]。对照组胰腺组织中可见大量胰岛细胞,而糖尿病模型组胰腺组织中胰岛细胞显著减少。模型组EAAT-3mRNA表达与对照组相比明显增加(P<0.01)。结论 EAAT-3高表达可能是糖尿病脑细胞损伤的主要机制。
Objective To investigate the expression of glutamate transporter (EAAT) in diabetic brain injury and its mechanism. Methods Twenty-eight Wistar rats were randomly divided into 2 groups (14 rats in each group): control group (conventional feeding) and model group (high glucose and fat feeding + STZ injection induced insulin resistance) Light cycle. After feeding for 1 month, blood sugar was measured. After 6 months, the mRNA expression of EAAT-1, EAAT-2 and EAAT-3 in rat cerebral cortex were detected by RT-PCR. Results The level of blood glucose [(20.016 ± 1.984) mmol / L] in diabetic model group was significantly higher than that in normal group (P <0.01) and in control group [(3.82 ± 0.123) mmol / L, P <0.01]. In the control group, a large number of islet cells were observed in the pancreatic tissue, while the islet cells in the pancreatic tissue of the diabetic model group were significantly reduced. The expression of EAAT-3mRNA in model group was significantly higher than that in control group (P <0.01). Conclusion High expression of EAAT-3 may be the main mechanism of diabetic brain injury.