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关键词：糖基化；糖基化反应终产物,高级
【摘要】 目的 为非酶糖基化(NEG)致衰老理论提供实验依据。 方法 利用D-半乳糖致小鼠衰老模型，通过血清中高级糖基化反应终产物(AGE)含量测定、自主运动试验、避暗试验、脾淋巴细胞增殖及白细胞介素-2(IL-2)诱生实验、超氧化物歧化酶(SOD)活力测定等检测NEG反应致衰老效应。 结果 正常衰老小鼠及D-半乳糖、L-葡萄糖处理的青年小鼠血清中AGE含量较高,分别为(6.21±1.84)、(5.87±1.70)及(5.75±1.36) U/ml, 青年对照组为(3.03±1.28) U/ml。D-半乳糖、AGE、L-葡萄糖都能引起类似衰老的效应。 结论 D-半乳糖的拟衰老效应是因其在体内引发了NEG反应及AGE诱发了大量的自由基放大NEG的效应而引起的，NEG反应是生物体衰老的一个重要原因。
The demonstration of the thesis ofnonenzymatic glycation inducing aging
SONG Xu , BAO Mingmin, LI Yongming,et al. * Institute of Medicinal Biotechnology, Chinese Academy of MedicalSciences, Beijing 100050
【Abstract】 Objective To prove thethesis of nonenzymatic glycation inducing aging. Methods Using D-galactose aging model, we measured the aging effects of D-galactose, L-glucose, advancedglycosylaton endproducts (AGE), and the inhibiting effect of aminoguanidine-HCL (AG) on D-galactose through determination of spontaneous motor activity, step-through test,proliferation rate of lymphocytes, IL-2 activity, and SOD activity. Furthermore, wedetected the AGE content in serum through specific ELISA. Results Wefound that D-galactose, L-glucose, and AGE all could cause the same effect as aging. AGcould inhibit the effect of D-galactose. Higher contents of AGE were detected in serum ofold mice and young mice given D-galactose or L-glucose. AG could lower the AGE contentproduced in the presence of D-galactose. Conclusions The agingeffect of D-galactose results from nonenzymatic glycation induced by galactose and theamplification of the production of free radicals and then of itself. Nonenzymaticglycation may play an important role in aging.
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