摘要
目的:观察力竭运动后大鼠海马NF-κB、BDNF在不同时间点的表达变化,探讨中枢神经系统的损伤及修复机制。方法:雄性SD大鼠70只,随机分为对照组(n=10)和力竭组(n=60)。力竭组进行6周力竭游泳训练后,选择0、4、8、12、16、24 h等不同时间点取脑,采用免疫组织化学和Western Blot技术观察海马内NF-κB、BDNF的表达变化。结果:(1)Western Blot结果显示:与对照组相比,力竭组海马内NF-κB含量在4 h开始升高(P<0.05),8 h达峰值(P<0.05),12~16 h开始回落(P<0.05),24 h恢复到正常水平(P>0.05)。力竭组海马内BDNF含量12 h及16 h组与对照组比较,BDNF的表达明显升高(P<0.05);(2)免疫组织化学结果显示:与对照组相比,力竭训练后0 h组大鼠海马内NF-κB表达以胞浆表达为主,4 h组核内表达逐渐增多(P<0.05),8 h组达高峰(P<0.05),12~24 h组核内表达逐渐减少(P>0.05)。海马内BDNF免疫阳性神经元则在力竭后24 h内持续表达且高于对照组(P<0.05),并于12 h达峰值(P<0.05),其余力竭各组之间差异无显著性(P>0.05)。结论:(1)大鼠力竭游泳运动可以活化海马内NF-κB信号转导系统,后者可能与运动性脑缺血再灌注时的神经细胞凋亡密切相关;(2)力竭运动可能通过诱导海马内BDNF的表达上调,对抗力竭运动性脑损伤,对神经元起到保护作用。
Objective: To observe the expression change of NF-κB and BDNF in the hippocampus of rats after exhausted swimming exercise at different times,and to investigate the mechanism unerlying the injury and repair of central nervous system.Methods: Seventy healthy SD rats were randomly divided into control group(n=10) and exhausted swimming group(n=60).The fresh cerebral tissues were divided on icewater bath while the paraform-perfused brains were obtained at 0,4,8,12,16 and 24 h after 6 weeks exhausted exercise,to respectively investigate the expression changes of NF-κB and BDNF in the hippocampus in rats by immunohistochemical techniques and Western Blot methods.Results:(1)Western Blot results showed that compared with control group,after exhausted exercise the expression of NF-κB in hippocampus increased at 4 h(P〈0.05),and peaked at 8 h(P〈0.05),decreased at 12~16 h(P〈0.05),and returned to normal levels at 24 h(P〈0.05).The expression of BDNF in hippocampus at 12 h and 16 h were significant higher than the control group(P〈0.05).(2) Immunohistochemical results showed that the expression of NF-κB was extremely lower and mainly located in cytoplasm in control group.Increased and transfered into nucleus at 4 h after exhausted exercise(P〈0.05),and reached peak levels at 8 h(P〈0.05),and gradually decreased at 12~24 h(P〉0.05).The number of BDNF positive cells increased in all exercise groups dramatically(P〈0.05),exclude 12 h group reached peak levels(P〈0.05),but there was no significant difference between other exhausted exercise groups(P〈0.05).Conclusion:(1) The NF-κB signaling pathway could be activated in hippocampus of rats by exhausted swimming exercise.It might be closely correlated reperfusion nerve cell apoptosis with active cerebral ischemia.(2) Exhausted exercise could up-regulate the expression of BDNF in hippocampus of rats,which might play an important role in preventing the brain impairments resulting from the exhausted exercise and in protecting the neurons of rat hippocampus.
出处
《神经解剖学杂志》
CAS
CSCD
北大核心
2012年第1期63-68,共6页
Chinese Journal of Neuroanatomy
基金
山西省自然科学基金(2011011034-2)
山东省自然科学基金(Y2008c29)
山西医科大学科技创新项目(01200803)