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从Tau蛋白过度磷酸化探讨2型糖尿病所致神经纤维化的机制
To investigate the molecular mechanism of neural fibrosis of patients with type 2 diabetes from the hyperphosphorylation of Tau
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DOI:
作者:
马玲,刘超
MA Ling, LIU Chao
作者单位:
长江大学附属第一医院内分泌科,天津市胸科医院麻醉科
Department of Endocrinology,the First Affiliated Hospital,Yangtze University; Department of Anesthesiology, Tianjin Thoracic Hospital.
关键词:
2型糖尿病;阿尔茨海默病;Tau 蛋白;过度磷酸化;罗格列酮
Type 2 diabetes; Alzheimer's disease; Tau protein; Hyperphosphorylation; Rosiglitazone
摘要:
【摘要】目的:观察胰岛素抵抗、高血糖和罗格列酮对大鼠认知能力、海马Aβ、Tau蛋白总量和磷酸化程度的影响,从Tau 蛋白过度磷酸化探讨2型糖尿病者神经纤维化的机制。方法:按随机单位组设2个干预因素,即2型糖尿病造模手段(3水平:普食喂养、高脂高糖高蛋白饮食、高脂高糖高蛋白饮食并腹腔注射小剂量链脲佐菌素)和药物干预(2水平:无处置、罗格列酮片按照3.0mg/Kg/d 灌胃4 周)的所有组合(3×2析因设计),48只SD大鼠分为6组。Morris水迷宫检测大鼠认识能力,葡萄糖氧化酶法检测血浆血糖,放免法检测血浆胰岛素,胰岛素抵抗指数HOMA-IR 评估胰岛素抵抗程度,取海马,高效液相色谱法检测谷氨酸浓度,ELISA检测Tau5(总Tau蛋白)和p-PHF1Ser396/404、p-AT8Ser199/202、p-12E8Ser262的表达。结果:胰岛素抵抗和2型糖尿病造成认知障碍,罗格列酮可缓解认知障碍;胰岛素抵抗和2型糖尿病可明显增加海马中谷氨酸(glutamate,Glu)浓度,罗格列酮可减少Glu浓度;胰岛素抵抗和2型糖尿病可增加海马中磷酸化Tau蛋白的表达;罗格列酮可减少海马中磷酸化Tau蛋白的表达。结论:胰岛素抵抗及血糖升高可能是2型糖尿病时海马Tau 蛋白过度磷酸化的原因;罗格列酮可以缓解这一过程。
【Abstract】Objective To observe the effect of insulin resistance, high blood sugar and rosiglitazone on the cognitive ability of rats and the content of A β and the degree of phosphorylation of Tau protein in the hippocampus, in order to investigate the mechanism of neural fibrosis of patients with type 2 diabetes from the hyperphosphorylation of Tau. Methods Groups of 2 intervention factors, namely, type II diabetes model method (3 levels: general diet, high fat and high sugar and high protein diet, high fat and high sugar and high protein diet and intraperitoneal injection of small dose of streptozotocin) and drug intervention (2 levels: no disposal, Rosiglitazone Tablets according to 3.0mg/Kg/d by gavage for 4 weeks) for all combinations (3 × 2 factorial design). 48 SD rats were divided into 6 groups. Morris water maze tests the cognitive ability of rats. Plasma glucose was determined by glucose oxidase method. The plasma insulin was determined by the method of radioimmunoassay. The degree of insulin resistance was evaluate by the insulin resistance index of HOMA-IR. The hippocampal tissue was taken out, and the concentration of glutamic acid was determined by HPLC, and the expression of Tau5 (Tau protein) expression and p-PHF1Ser396/404, p-AT8Ser199/202, p-12E8Ser262 was determined by ELISA. Results Insulin resistance and type 2 diabetes cause cognitive impairment. Rosiglitazone can alleviate cognitive impairment. Insulin resistance and type 2 diabetes can significantly increase the concentration of Glu in the hippocampus. Rosiglitazone can reduce the concentration of Glu. Expression of insulin resistance and type 2 diabetes increased the phosphorylation of Tau protein in the hippocampus. Rosiglitazone can reduce the expression of Tau protein phosphorylation in hippocampus. Conclusion Insulin resistance and elevated blood sugar may be the cause of the phosphorylation of Tau protein in the hippocampal of 2 type diabetic rats. Rosiglitazone can mitigate this process.
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