期刊
BIOMEDICAL AND ENVIRONMENTAL SCIENCES
卷 23, 期 2, 页码 161-166出版社
CHINESE CENTER DISEASE CONTROL & PREVENTION
DOI: 10.1016/S0895-3988(10)60047-5
关键词
Salidroside; Aging; D-galactose
资金
- National Grand Fundamental Research 973 Program of China [2007CB507406]
- National Natural Science Foundation of China [30600659]
- Central and Non-profitable Basic R&D Funds for Scientific Research Institutes [IMBF200913]
Objective To investigate the protective effects of putative AGEs (advanced glycation endproducts) inhibitor salidroside against aging in an accelerated mouse aging model induced by D-galactose. Methods A group of 5-month-old C57BL/6J mice were treated daily with D-galactose, D-galactose combined with salidroside, salidroside alone, and control buffer for 8 weeks. At the end of the treatment, serum AGEs levels, neurological activities, expression of glial fibrillary acidic protein (GFAP) and neurotrophin-3 (NT-3) in the cerebral cortex, as well as lymphocyte proliferation and IL-2 production were determined. Results D-galactose induced mouse aging model was developed as described before. As expected, salidroside blocked D-galactose induced increase of serum AGEs levels. It also reversed D-galactose induced aging effects in neural and immune system, as evidenced by improving motor activity, increasing memory latency time, and enhancing lymphocyte mitogenesis and interleukin-2 (IL-2) production. Furthermore, elevated expression of GFAP and NT-3 in the aged model mice was also reduced upon salidroside treatment. Conclusion Salidroside inhibits AGEs formation in vivo, which at least partially contributes to its anti-aging effect in D-galactose induced aging model.
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