摘要
目的探讨烟碱对Alzheimer病(AD)的防治作用及机制。方法将Aβ25-35注射于大鼠海马部位建立AD和烟碱AD动物模型,通过Morris水迷宫试验评定大鼠学习记忆功能,采用免疫组化、ELISA方法,分别检测大鼠海马部位GFAP免疫染色阳性星形胶质细胞形态和细胞因子IL-1β含量变化。结果在平台定位航行试验中,正常对照组、烟碱AD组潜伏期随训练天数的增加而逐渐缩短,而AD组潜伏期无明显缩短的变化趋势。正常对照组在平台象限的游泳时间百分比和游泳距离百分比分别为64.94%、52.36%,烟碱AD组分别为54.67%、50.41%,AD组分别为22.34%、26.92%,烟碱AD组与AD组相比差异显著。AD组大鼠海马部位GFAP免疫染色阳性星形胶质细胞数较烟碱AD组大鼠明显增多。注射Aβ25-35后第1天、第7天、第15天,AD组大鼠海马IL-1β含量为(84.98±15.47)pg/mg、(92.58±17.01)pg/mg、(77.14±18.81)pg/mg;烟碱AD组海马IL-1β含量为(49.74±15.56)pg/mg、(41.46±12.37)pg/mg、(32.96±9.68)pg/mg。AD组海马IL-1β含量较烟碱AD组大鼠明显升高,差异显著。结论烟碱具有抑制Aβ对星形胶质细胞的激活,使星形胶质细胞分泌炎性细胞因子IL-1β减少,改善AD大鼠认知功能的作用。
To explore the mechanism of nicotine-induced improvement in AD. Methods The Aβ25-35 was injected into bilateral hippocampus to establish AD rat models and nicotine-AD rat models. The learing and memory function among AD rats and nicotine-AD rats were evaluated by the water maze test. The GFAP immunoreative astrocytes were stained by immunohistochemistry. The IL-1β levels of the hippocampal tissues were tested by ELISA. Results In the water maze test, normal control groups and nicotine-AD groups learned to locate a hidden platform as indicated by progressively shorted latencies across training days, however, AD groups were no progressively shorter latencies. Time and distance percentage spent in platform quadrant were calculated, normal control groups were 64.94% ,52.36%, nicotine-AD groups were 54.67%,50.41%, AD groups were 22.34%,26.92%, respectively. The GFAP immuonreactive astrocytes in AD groups were increased than those in nicotine-AD groups and normal control groups. The IL-1β levels of the hippocampal tissues in AD groups were significantly higher than those in nicotine-AD groups and normal control groups. Conclusion Nicotine may inhibite the astrocyte activation-induced by Aβ25-35, decrease the secretion of astrocyte-derived IL-1β and improve cognitive function of AD rat.
出处
《重庆医学》
CAS
CSCD
2007年第16期1619-1621,F0002,共4页
Chongqing medicine
