摘要
目的:观察丙泊酚衍生物cqmu-039对大鼠脑缺血再灌注损伤的保护作用,探讨cqmu-039对脑缺血再灌注的保护机制。方法:雄性SD大鼠40只,随机分为假手术组、模型组、药物低、中、高(6、12、24 mg/kg)剂量组。模型组采用大脑中动脉栓塞法(middle cerebral artery occlusion,MCAO)线栓法制备脑缺血模型,缺血2 h后再灌注24 h取脑;假手术组与模型组采用相同手术方法,不植入栓子,药物处理组系在脑缺血模型建立后立即腹腔注射给药。结果:与模型组相比,药物处理组能显著改善大鼠神经缺损症状,其行为学评分降低,脑梗死面积明显缩小,皮层、CA1区与CA3区治疗组大鼠胶质细胞源性神经营养因子(lial cell line-derived neurotrophic factor,GDNF)阳性细胞数量明显增加(P<0.05,P<0.01,P<0.01);CA1区、CA3区及齿状回胶质原纤维酸性蛋白(glial fibrillary acidic protein,GFAP)表达明显减少。结论:丙泊酚衍生物cqmu-039能通过提高GDNF表达同时降低GFAP的表达从而明显改善大鼠脑缺血再灌注时的损伤。
Objective：To investigate the protective effects of propofol derivative cqmu-039 on cerebral ischemia-repeffusion injury in SD rats and its mechanisms. Methods ：A total of 40 SD rats were randomly divided into 5 groups：sham surgery group, cerebral isehemia-reperfusion（IR） model group,low（6 mg/kg）,medium（12 mg/kg） and high（24 mg/kg） doses of eqmu-039 groups. IR model was generated via the surgery of middle cerebral artery ocelusion（MCAO） for 2 h and then repeffusion of blood for 24 h. Sham surgery was performed in the same way as IR model without implanting the embolus. Three different doses of eqmu-039 were injected immediately after the IR surgery was performed. Protective effects of eqmu-039 were evaluated through the neurological behavioral score, 2,3,5-triphenyltetrazolium chloride （TrC） staining and expressions of glial cell derived neurotrophie factor（GDNF） and glial fibrillary acidic protein（GFAP） in the hippoeampus. Results：Neuronal injury was significantly improved in eqmu-039 groups than in model group. In addition, lower neurological behavioral scores, smaller cerebral infarct size and higher expressions of GDNF in CA1, CA3 and cortex regions were observed in eqmu-039 groups than in model group（P〈0.05 ,P〈0.01 ,P〈0.01）. Expressions of GFAP in CA1, CA3 and dentate gyms regions in eqmu-039 groups were deereasent in a dose-dependent manner. Conelusions：Propofol derivative cqmu-039 can effectively improve cerebral ischemia-reperfusion injury of rats through increasing expressions of GDNF and decreasing expressions of GFAP.
出处
《重庆医科大学学报》
CAS
CSCD
北大核心
2013年第3期265-269,共5页
Journal of Chongqing Medical University
基金
重庆市科委自然科学基金重点资助项目(编号:CSTC2009BA5086)
