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作 者:杨德刚[1,2] 李建军[1,3,4,2] 杨明亮[1,2] 杜良杰[1,2] 胡安明[1,2] 顾蕊[3,2] 陈亮[1,2] 褚宏宇[1,2] 张宪娣[4,2] 吴海丰[4,2]
机构地区:[1]中国康复研究中心北京博爱医院脊柱脊髓神经功能重建科,北京市100068 [2]首都医科大学康复医学院,北京市100068 [3]中国康复研究中心北京博爱医院骨科,北京市100068 [4]中国康复研究中心北京博爱医院科教处,北京市100068
出 处:《中国康复理论与实践》2015年第4期382-386,共5页Chinese Journal of Rehabilitation Theory and Practice
基 金:国家自然科学基金项目(No.81272164);中央级公益性科研院所基本科研业务费专项资金项目(No.2011CZ-2)
摘 要:目的观察脊髓切开术干预后大鼠脊髓损伤区自噬活性的变化。方法 54只成年雌性Sprague-Dawley大鼠随机分为假手术组(n=18)、挫伤组(n=18)和手术组(n=18)。用NYU打击器制备T10脊髓挫伤模型。手术组在造模后24 h行脊髓切开术。在伤后第1、7、14天,采用开放场地试验评估大鼠运动功能;RT-PCR检测Beclin-1和Bcl-2的m RNA表达;伤后3 d开始电镜观察自噬体。结果损伤后7 d、14 d,手术组大鼠BBB评分高于挫伤组(P<0.05),Beclin-1 m RNA水平低于挫伤组(P<0.05);伤后3 d、7d,Bcl-2 m RNA水平高于挫伤组(P<0.05)。伤后7 d、14 d,大鼠脊髓损伤区的Beclin-1 m RNA水平与行为学评分负相关(P<0.01)。脊髓挫伤后自噬体形成增多,手术组自噬体形成减少。结论脊髓切开术能改善创伤性脊髓损伤大鼠的运动功能,可能与抑制自噬、上调Bcl-2 m RNA表达有关。Objective To observe the effects of myelotomy on autophagy activation after traumatic spinal cord injury(SCI) in rats.Methods 54 adult female Sprague-Dawley rats were randomly assigned to sham-operated group(SG, n=18), contusion group(CG, n=18) or myelotomy group(MTG, n=18). The T10 SCI model in rats was induced with a New York University(NYU) impactor and myelotomy was performed 24 hours after SCI. They were evaluated with the BBB score 1, 7, 14 days after injury. The expression of m RNA of Beclin-1 and Bcl-2 were detected with real-time quantitative reverse transcriptase polymerase chain reaction(RT-PCR). The formation of autophagosome was investigated under electronic microscope(EM) 3 days after injury. Results BBB score was more in the MTG than in the CG 7 and 14 days after injury(P〈0.05), while the expression of Beclin- 1 m RNA was less(P〈0.05). The expression of Bcl- 2 m RNA was more in the MTG than in the CG 3 and 7 days after injury(P〈0.05). The expression of Beclin-1 m RNA was negatively correlated with BBB scores(P〈0.05). The formation of autophagosome was less in the MTG than in the CG. Conclusion Myelotomy can improve the recovery of motor function in rats after acute traumatic SCI, which may associate with neuroprotection mediated by inhibition of autophagy through the Bcl-2signaling pathway.
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