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作 者:冯亮[1] 徐辰[2] 郑浩[1] 沈文娟[1] 吕俊华[1]
机构地区:[1]暨南大学药学院药理教研室,广东广州510632 [2]澳门理工学院高等卫生学校
出 处:《中国老年学杂志》2008年第13期1251-1254,共4页Chinese Journal of Gerontology
基 金:澳门科技发展基金资助(035/2005/A)
摘 要:目的研究茶多酚(tea polyphenols,TP)对D-半乳糖诱导的糖基化大鼠并发脑损害的干预作用。方法D-半乳糖(150mg·kg-1·d-1)腹腔注射给药造模8w,诱导形成糖基化大鼠,并在造模第3周时分为模型组,氨基胍组,茶多酚高、中、低剂量后,灌胃给药6w。测定红细胞醛糖还原酶活性、糖化血红蛋白、血清果糖胺和晚期糖基化终末产物(AGEs)含量;脑组织中AGEs含量、SOD活性和MDA含量及脑神经细胞内钙离子水平,透射电镜观察海马神经细胞线粒体的变化。结果茶多酚高、中剂量组能明显降低模型大鼠红细胞醛糖还原酶活性,抑制糖化产物的形成,降低脑组织中AGEs及脑细胞内钙的含量,提高SOD活性,降低MDA含量,保护海马神经细胞线粒体结构的完整性。结论茶多酚具有抑制D-半乳糖诱导的糖基化反应,并对糖基化状态并发的脑神经细胞损害具有保护作用。Objective To investigate the effect of tea polyphenols (TP) on brain damage in rats model of glycation induced by D- galactose (D-gal). Methods Rats were injected with D-gal (150 mg ·kg-1·d-1,ip) for 8 weeks. From the 3rd week, TP (150,75, 37.5 mg·kg-1·d-1 ) were administrated for 6 weeks. The activity of aldose reductase, the levels of fructosamine in serum, the amount of glycosylated hemoglobin and advanced glycation end-products (AGEs) in plasma ;the activities of SOD, MDA, the level of AGEs in brain and intracellular calcium level in cranial nerve cell were measured. Furthermore, the hippocampal tissues were collected to observe the changes of mitochondria under electronic microscopy. Results In high,medium dose TP groups,the activity of aldose reductase,the level of AGEs in brain, intracellular calcium level in brain and the level of MDA decreased ( P 〈 0. 01 ,P 〈 0. 05 ). However,the activity of SOD increased ( P 〈 0. 01,P 〈 0. 05 ). Besides, integration of structure of the mitochondria in hippocampal tissue was protected. Conclusions TP can inhibit glycation reaction induced by D-gal and protect the damage of cranial nerve cell caused by glycation.
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