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作 者:郭树章[1] 任先军[1] 蒋涛[1] 欧阳忠[1]
机构地区:[1]第三军医大学新桥医院骨科
出 处:《中国矫形外科杂志》2005年第22期1730-1732,共3页Orthopedic Journal of China
摘 要:[目的]探讨NT3(神经营养素3)对脊髓损伤保护作用的机制。[方法]105只SD大鼠随机分为3组:对照组(生理盐水组),实验组(NT3组)和假手术组,每组35只,各分为7个时相点,每个时相点5只大鼠。采用Allen’s法以30gcm力致伤大鼠T8脊髓,经蛛网膜下腔导管分别于术后0、4、8、12、24h、3、7d各注入NT3溶液200ng与生理盐水组和假手术组对照,于术后4、8、12、24h、3、7、14d自右心室取血用比色法测定血清中的一氧化氮合成酶活性。[结果]大鼠脊髓损伤后一氧化氮合成酶(NOS)升高,术后12h达高峰,实验组NOS水平及升幅明显低于对照组。[结论]NT3能有效抑制NOS在脊髓损伤后的活性,从而减少了NO的生成,这可能是促进大鼠脊髓损伤后运动功能恢复的作用机制之一。[ Objective ] To investigate the protective mechanism of neurotrophin-3 (NT-3) in spinal cord injury (SCI). [ Method] One hundred and five SD rats were randomly divided into 3 groups:control group (saline group), experimental group ( NT-3 group) and sham group. SCI in SD rats was created with Allen's method by a 30 gcm impacting on the posterior T8 spinal cord. NT-3 was grafted into the subarachnoid space of the rats in treatment group immediately and 4,8,12, 24 h and 3,7 d after spinal cord injury. The nitricoxidesynthase (NOS) activity in rats blood were assayed with colorimetric methods in 4,8,12,24 h and 3,7,14 d. [ Result] Abnormal activity expression of NOS was detected in serum of injured rats, and reached peak at 12 hours after the injury. The level of NOS activity in NT-3 group was significantly lower as compared with that in control saline group. [ Conclusion] NT-3 can protect spinal cord from injury in vivo,and inhibit abnormal expression of nitricoxidesynthase (NOS), thus the neurotoxicity of excessive nitricoxide(NO) is abated.
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