机构地区:[1]山西医科大学人体解剖学教研室,太原030001 [2]烟台大学体育学院,烟台264005
出 处:《神经解剖学杂志》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)
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
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