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作 者:王小阳[1] 朱长连[1] 邱林[1] 徐发林[1] 程秀永[1]
出 处:《郑州大学学报(医学版)》2003年第1期30-33,共4页Journal of Zhengzhou University(Medical Sciences)
基 金:河南省重大科技攻关资助项目 0122032100;河南省高等学校创新人才基金资助项目
摘 要:目的:探讨二甲亚砜(DMSO)对新生大鼠缺氧缺血性脑损伤的保护作用及其可能机制。方法:7 d wistar大鼠缺氧缺血(HI)后2 h和12 h侧脑室内注射DMSO(n=39)或安慰剂(PBS)(n=39);缺氧缺血后24 h,DMSO组和安慰剂组各6只,正常对照组6只,取脑分离左右半球进行匀浆,用于微管相关蛋白2(MAP-2)和胞衬蛋白(fo-drin)Western印迹检测;缺氧缺血后72 h,DMSO和安慰剂组各33只,正常对照组6只,经心脏灌注固定取脑,用MAP-2免疫组化和HE染色,计算脑梗死体积和脑损伤积分。结果:DMSO组大脑各部位梗死体积和脑损伤积分均低于PBS组,其中以大脑皮层的变化最明显;DMSO组MAP-2和胞衬蛋白的降解产物均少于安慰剂组,其中以M,为150 000/145 000降解产物减少最明显。结论:DMSO具有脑保护作用,其机制可能与抑制钙依赖蛋白酶有关。Aim : To study the protective effects and possible mechanism of dimethyl sulfoxide( DMSO) on neonatal rat hypoxia-ischemia( HI) brain damage. Methods:Unilateral cerebral HI was induced in 7-day old rats by ligation of the left carotid artery and hypoxia for 55 min. DMSO (re =39) or vehicle (PBS) (n = 39) was injected intraparenchymaly by u-sing a syringe attached to a microinjection pump at 2 h and 12 h post-HI. For immunoblotting of microtubule associated pro-tein-2 (MAP-2) and fodrin, pups in normal control group as well as those in DMSO and vehicle groups (n =6, for each group) were sacrificed at 24 h post-HI. For MAP-2 immunostaining and hematoxylin-eosin staining, pups (n =33, for DMSO and vehicle group; n =6 in normal control group) were sacrificed at 72 h post-HI. Results; Infarct volume and brain injury scoring in different brain regions reduced after treated by DMSO compared with vehicle group, especially in cortex. The breakdown products of MAP-2 and fodrin were inhibited after DMSO treatment compared with vehicle group, especially the calpain dependent 150 000/145 000 fodrin breakdown products. Conclusion: DMSO has neuroprotective effects in neonatal HI brain damage. One of the mechanisms might be correlated with inhibition of calpain.
关 键 词:二甲亚砜 脑缺血 脑保护 新生儿缺氧缺血性脑病 HIE
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