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目的研究糖尿病发展过程中大鼠血浆β-淀粉样蛋白42(amyloid beta 42,Aβ42)、胰岛素和血糖的动态变化;初步探讨在糖尿病发展过程中胰岛素和血糖对Aβ42的影响,并分析糖尿病发展成为认知障碍的风险。方法腹腔注射链脲佐菌素(streptozotocin,STZ)复制实验性糖尿病大鼠模型,以血糖浓度≥16.7 mmol·L-1确定模型成立。实验分为正常组与模型组。建模前后共采集5次血液,每次间隔15 d。建模60 d,代谢笼测大鼠24 h食量、水量、尿量和粪便量;建模70 d,八臂迷宫实验测定大鼠觅食时间、参考记忆错误次数和工作记忆错误次数。用葡萄糖氧化酶法和酶联免疫吸附法测血糖、胰岛素和Aβ42的含量。结果 STZ复制的糖尿病大鼠模型稳定。模型组大鼠食量、水量、尿量和粪便量明显高于对照组(P<0.01);八臂迷宫实验:与对照组比较,模型组大鼠觅食时间、参考记忆错误频率和平均探究时间均有显著性差异(P<0.05),工作记忆错误频率高于对照组,但是无统计学意义。模型成立初期Aβ42随胰岛素增多而降低,建模45 d,Aβ42含量最高,之后下降。结论建模70 d,模型组大鼠学习记忆能力明显低于对照组,糖尿病大鼠患认知障碍的风险明显增高;糖尿病初期,模型成立45~75 d,为给予药物干预治疗的最佳时期;临床上可以通过同时检测胰岛素和Aβ42判断糖尿病是否向认知障碍发展。
Objective To investigate the dynamic changes of plasma amyloid beta 42, insulin and glucose in rats during the development of diabetes mellitus. To explore the effects of insulin and blood glucose on Aβ42 during the development of diabetes mellitus, Risk of cognitive impairment. Methods Experimental diabetic rat models were established by intraperitoneal injection of streptozotocin (STZ). The model was established by blood glucose concentration ≥16.7 mmol·L-1. The experiment was divided into normal group and model group. A total of 5 blood samples were taken before and after modeling, with an interval of 15 days. The food intake, water volume, urine output and stool volume of the rats for 24 h were determined by metabolic cage test after 60 days. The foraging time, the number of reference memory errors and the number of working memory errors of rats were determined by the eight-arm maze test after modeling for 70 days. Glucose, insulin and Aβ42 were measured by glucose oxidase and enzyme-linked immunosorbent assay. Results STZ-induced diabetic rat model was stable. The food intake, water volume, urine output and stool volume in model group were significantly higher than those in control group (P <0.01). Eight-armed maze test: Compared with control group, the feeding time, frequency of reference memory error and mean time to explore (P <0.05), working memory error frequency higher than the control group, but no statistical significance. Aβ42 decreased with the increase of insulin in the initial stage of model establishment. After modeling for 45 days, the content of Aβ42 was the highest, then decreased. CONCLUSIONS: After 70 days of modeling, the learning and memory abilities of rats in the model group were significantly lower than those in the control group. The risk of cognitive impairment was significantly increased in diabetic rats. In the initial stage of diabetes, the model was established 45-75 days, which was the best time for drug intervention Clinically, simultaneous detection of insulin and Aβ42 can determine whether diabetes develops into cognitive impairment.