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作 者:黄柏南[1] 孙善全[1] 汪克建[1] 李红岩[1] 杨美[1]
机构地区:[1]重庆医科大学基础医学院神经生物学研究室,重庆400016
出 处:《基础医学与临床》2007年第11期1198-1202,共5页Basic and Clinical Medicine
基 金:国家自然科学基金(30270437);教育部春晖计划(2004)
摘 要:目的观察在大鼠脊髓缺血再灌注损伤(SCII)过程中内质网分子伴侣GRP78的表达变化,并探讨其意义。方法健康成年Wistar大鼠55只,随机分为两组:(1)脊髓压迫缺血再灌注组50只,每个时间点10只,采用自制压迫装置制备脊髓压迫缺血再灌注模型;(2)假手术对照组5只,只做全椎板切除不做脊髓压迫。用免疫组化、West-ernblot和TUNEL等方法,分别于缺血再灌注后30min、3、7、11和23h,检测压迫段脊髓组织中GRP78的表达变化及细胞凋亡情况。结果再灌注30min后,GRP78在压迫段脊髓开始表达上调,7h达峰值,11h表达回落,23h显著减少。TUNEL染色显示,神经细胞的凋亡指数随着再灌注时间的延长而升高。结论GRP78在脊髓缺血再灌注损伤中呈现时序性的表达变化,这可能是脊髓内源性保护机制之一。Objective To evaluate the changes of GRP78 expression in the Spinal Cord of Ischemia/Reperfusion Injuried Rat. Methods Fifty five adult Wistar rats (250 -300 g) were randomly divided into 2 groups as control group (n = 5 ) and operation group (n = 50 ). The spinal cord SCII model was established. The expression of GRP78 was detected in spinal cord tissue through immunohistochemistry(IHC) and Western blot analysis, and the neuronal apoptosis was detected through terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) methods. Results The GRP78 expression was increased at 30 min of reperfusion, and peaked at 7 h, but began to decline at 11 h post-reperfusion, and reduced significantly at 23 h. The number of GRP78 positive neurons at 0. 5, 3,7,11 and 23 h groups was( 19. 4 ± 1.34), (42. 6 ± 2. 30), ( 82. 4 ± 2. 07 ), ( 40. 0 ± 1.58 ) and ( 18.8±0. 83 ), respectively and significantly higher than that of control group ( P 〈 0. 05 ). TUNEL staining showed that the apoptotic index was gradually elevated with increasing time period. Conclusion The data strongly suggested that GRP78 expression was drastically increased in the SCII model which showed a time-dependent manner. This might be one of the endogenous protective mechanisms.
关 键 词:内质网分子伴侣GRP78 再灌注损伤 脊髓损伤 大鼠
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