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目的基于代谢组学方法研究应激性高血压大鼠尿液中的差异性代谢组份,并通过差异性代谢组份探讨应激性高血压的发病机制,为进一步进行应激性高血压大鼠的药物治疗提供实验依据.方法♂Wistar大鼠20只分为正常对照组与应激性高血压模型组,正常对照组未行任何处理,应激性高血压模型组大鼠给予足底电刺激、制动、夹尾等刺激.用大鼠尾动脉测压仪尾套法测各组大鼠尾动脉收缩压确定应激性高血压模型建立成功后,收集各组大鼠尿液,通过核磁共振氢谱法测出各组大鼠尿液中差异性代谢组份.结果(1)通过足底电刺激足底电刺激、制动、夹尾等复合刺激方法可以建立应激性高血压模型;(2)与正常组相比,应激性高血压模型组大鼠尿液中酪氨酸、苯丙氨酸、丙酮、1-甲基组氨酸、β-葡萄糖、乙酸-醋酸盐、甲酸、乙酰乙酸、丙二酸、柠檬酸、苹果酸、肌酸酐、肌酸、尿素的含量增加.结论应激性高血压大鼠存在脂类、氨基酸、糖代谢异常.
OBJECTIVE: To study the differential metabolites in urine of stress-induced hypertensive rats based on metabonomics and explore the pathogenesis of stress-induced hypertension by differential metabolites. To further investigate the effects of stress-induced hypertension 20 rats were divided into normal control group and stress-induced hypertension model group, without any treatment in normal control group. Rats in stress-induced hypertension group were given foot-end-organ Stimulation, braking, tail-tails and other stimuli.Using the tail cuff of rat tail artery to measure the systolic pressure of the caudal artery in each group to determine the stress-induced hypertension model.After successful establishment of the model, urine of each group was collected and passed through Nuclear magnetic resonance (1H-NMR) spectroscopy was used to detect the differential metabolites in the urine of rats in each group.Results (1) The stress-induced hypertension (2) Compared with the normal group, the urinary tyrosine, phenylalanine, acetone, 1-methylhistidine, β-glucose, acetic acid-acetic acid Salt, formic acid, acetoacetic acid, malonic acid, citric acid, malic acid, creatinine, muscle Acid and urea increased.Conclusion There exists lipids, amino acids and glucose metabolism abnormalities in stress-induced hypertensive rats.