超低频经颅磁刺激对脑缺血大鼠认知功能的影响及机制

摘要

Objective To study the influence of ultralow‐frequency transcranial magnetic stimulus(TMS) on the cognitive a‐bility of rats with cerebral ischemia and its mechanism .Methods 60 healthy rats were divided into 4 groups(15 cases each):A (sham‐operation) ,B(model) ,C(TMS) and D(TMS+ H89) .The escape latency time ,times of passing through platform ,expression level of VEGF ,BDNF and nestin protein were compared among 4 groups .Results In the group A ,the escape latency time was (16 .31 ± 2 .33)s ,times passing through platform were (8 .02 ± 1 .76) times ;in group B ,which were (57 .14 ± 2 .89)s and (3 .15 ± 0 .88) times;in group C ,which were (29 .18 ± 1 .95)s and (5 .44 ± 0 .75) times ;in group D ,which were (45 .87 ± 2 .06)s and (4 .16 ± 1 .02) times .Compared with the group A ,the escape latency time in the group B ,C and D was significantly extended ,more‐over that in the group B was longer than that in the group D and C ,the differences were statistically significant (P<0 .05);the times of passing through platform decreased ,which in the group B was less than that in the group D and C ,the differences had sta‐tistical significance(P<0 .05) .The expression levels of VEGF ,BDNF and nestin had statistical differences among various groups (P<0 .05) .Conclusion Low‐frequency TMS can significantly improve the cognitive ability of rats with cerebral ischemia ,its effect is related to the expression of cAMP‐response element binding protein and its following genes(VEGF and BDNF) .%目的：研究超低频经颅磁刺激（TMS）对脑缺血大鼠认知功能的影响并探讨其机制。方法将60只健康大鼠分为4组（各15只）：A组（假手术组），B组（模型组），C组（TMS组）和D组（TMS＋H89组）。比较各组大鼠的逃避潜伏时间、跨越原平台次数及血管内皮生长因子（VEGF）、脑源性神经营养因子（BDNF）和巢蛋白（nestin）的表达水平。结果A组大鼠逃避潜伏期为（16．31±2．33）s，跨越原平台次数为（8．02±1．76）次；B组大鼠逃避潜伏期为（57．14±2．89）s，跨越原平台次数为（3．15±0．88）次；C组大鼠逃避潜伏期为（29．18±1．95）s，跨越原平台次数为（5．44±0．75）次；D组大鼠逃避潜伏期为（45．87±2．06）s，跨越原平台次数为（4．16±1．02）次。与A组比较，B、C、D组大鼠的逃避潜伏期明显延长，且B组长于D组及C组，差异均有统计学意义（P＜0．05）；大鼠的跨越原平台次数明显减少，且B组少于D组及C组，差异均有统计学意义（P＜0．05）。各组大鼠VECF、BDNF和nestin表达水平比较，差异均有统计学意义（P＜0．05）。结论低频TMS可以明显改善脑缺血大鼠的认知功能，其作用与环磷腺苷效应元件结合蛋白及其下游基因（VEGF、BDNF）的表达有关。