锁阳多糖咀嚼片对衰老模型大鼠NO代谢及免疫功能的影响

目的探讨锁阳多糖咀嚼片对D-半乳糖致衰老大鼠血、脑、肾一氧化氮(NO)代谢及免疫器官功能的影响。方法提取并制备锁阳多糖、锁阳水提取物咀嚼片;Wistar大鼠随机分为空白对照组、衰老模型组、维生素E对照组、锁阳多糖咀嚼片组、水提物咀嚼片组。以D-半乳糖建立衰老大鼠模型,经药物干预后,检测各组大鼠血、脑、肾组织中NO的含量,脾脏指数、胸腺指数;观察脾脏组织的病理形态学变化。结果衰老模型大鼠血、脑、肾中NO含量异常增加,脾脏指数、胸腺指数下降,脾脏发生明显病理损伤。锁阳多糖咀嚼片能明显降低血、脑、肾中异常升高的NO含量,提高脾脏指数、胸腺指数,改善脾脏的病理损伤。并且锁阳多糖咀嚼片组对NO作用优于锁阳水提取咀嚼片组。结论锁阳多糖咀嚼片可通过调节衰老模型大鼠的NO代谢水平、提高免疫功能而发挥抗衰老作用。

Effects of Cynomorium Polysaccharide Chewable Tablets on NO Metabolism and Immune Function of D - galactose - induced Aging Rats

Objective To explore the effects of Cynomorium polysaccharide chewable tablets on metabolism of NO in blood,brain and kidney,and in the function of immune organs in D-galactose-induced aging rats. Methods The chewable tablets of Cynomorium polysaccharide and Cynomorium water extract were prepared. Wistar rats were randomly divided into normal control group,aging model group,Vit E group,Cynomorium polysaccharide chewable tablets group,Cynomorium water extract chewable tablets group. The aging rats model was established by hypodermic injection of D-galactose .After administration,the content of nitric oxide (NO) in blood,brain and renal tissue,and the index of spleen and thymus in each group were detected. Meanwhile,the pathological morphological changes of spleen were also observed. Results Compared with the normal control group,the content of NO in blood,brain and renal tissue increased significantly,the spleen index and thymus index decreased significantly,and there was obviously pathological injury of spleen in aging model group.Cynomorium chewable tablets decreased NO level in blood,brain and renal tissue of the aging rats,increased the spleen index and the thymus index,and relieved the spleen pathological injury of aging rats significantly. The effect of Cynomorium polysaccharide chewable tablets group on improving the metabolism of NO was superior to that of water extract group. Conclusion Cynomorium polysaccharide chewable tablets play an anti-aging role by regulating the metabolism of NO and improving the immune function of D-galactose-induced aging rats.