| Gerontological studies performed at the organismic, cellular, and molecular levels have generated numerous theories that attempt to explain the events leading to biological senescence. Now many studies have focused on the theory of nonenzymatic glycation (NEG) inducing aging which was proposed by Cerami A in 1985. It has been reported by many researchers that elevated level of AGE in vivo may accelerate aging process in animals and humans. Indeed, the AGE formation inhibitor, aminoguanidine, could prevent certain age-associated changes in aging model. In order to provide more direct evidence for the hypothesis that NEG is involved in the pathogenesis of aging, and to investigate the role of NEG in the process of immunological senescence, three groups of two-month-old C57 mice were injected daily and severally with D-galactose, D-galactose modified lysine (AGE), D-galactose plus aminoguanidine(an specific AGE formation inhibitor), for 60 days. Young and old control groups were administrated buffer. The ultrastructure changes of thymus and spleen were investigated, as well as the changes in the production of cytokines by splenic lymphocytes. According to the theory of NEG inducing aging, in vitro screening model of NEG inhibitor was established and applied in the NEG inhibitor screening from components of Chinese traditional medicine and synthetic chemical compounds. Positive samples were obtained and the in vivo effects were investigated.Within the period of treatment, all groups of mice gained weight normally. Serum AGE levels was determined by AGE-ELISA. As anticipated, old mice treated with PBS had an higher level of serum AGEs than that of young mice (P < 0.01). Young mice treated with D-galactose, AGE showed an increased level of serum AGEs comparing with young control mice (P < 0.01 or 0.05). AG, however, could prevent AGE increase in D-galactose treated mice(P < 0.05).Electron microscopy of thymus and spleen demonstrsted that old mice,... |
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