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作 者:赵彬[1] 何志义[1] 吴晓黎[1] 刘晓梅[1]
机构地区:[1]中国医科大学附属第一医院神经内科,辽宁沈阳110001
出 处:《中国现代医学杂志》2007年第19期2359-2361,2365,共4页China Journal of Modern Medicine
基 金:辽宁省自然科学基金资助项目(20032054)
摘 要:目的研究经颈内动脉注射质粒PLXSN介导人Bcl-2基因对大鼠局灶性脑缺血后脑梗死体积,神经细胞凋亡及Bcl-2、Bcl-xl和Bax表达的影响。方法健康Wistar雄性大鼠72只,采用线栓法制备大鼠MCAO模型,随机分为空质粒PLXSN对照组和PLXSN-Bcl-2治疗组。再灌注3h后分别经颈内动脉注射质粒PLXSN、PLXSN-Bcl-2。采用TTC染色法检测脑梗死体积,TUNEL法标记凋亡细胞,免疫组织化学法检测Bcl-2、Bcl-xl、Bax蛋白表达。结果MCAO后24、48和72h,脑梗死体积和凋亡神经细胞率治疗组显著小于对照组(P<0.05和P<0.01),治疗组Bcl-2和Bcl-xl蛋白的表达较对照组显著增加(P<0.01和P<0.05),而Bax蛋白表达治疗组较对照组显著减少(P<0.05)。结论颈内动脉注射质粒PLXSN介导Bcl-2基因对脑缺血有脑保护作用。促进bcl-2、bcl-xl表达升高,下调bax蛋白表达,从而抑制神经细胞凋亡,可能为其治疗脑梗死的机制之一。[Objective] To observe the infarct volume, neuronal apoptosis and related genes expression alter cerebral isehemia by intra-carotid artery delivery of pLXSN-Bel-2 eDNA. [Methods] 72 male wistar rats were made into MCAO models and randomly assigned into pLSXN control group and Bel-2 gene treated group. Two groups were respectively intra-earotid delivery of pLXSN and pLXSN-Bel-2 three hours after MCAO. We studied the infarct volumes, neuronal apoptosis and Bel-2, Bcl-xl, Bax expression in 24, 48 and 72 h after MCAO. [Results] In 24, 48, 72 h after MCAO, the infarction volume and neuronal apoptosis in treated group were significantly less than the control group (P 〈0.05 and P 〈0.01, respectively). Compare with the control group, the expression of Bcl-2 and Bel-xl proteins in treated group signitleanfly increased (P 〈0.01 and P 〈0.05, respectively), but Bax proteins in treated group signiticanfly decreased (P 〈0.05). [Conclusions] This study indicates that bel-2 gene produces neuroproteetive effect by intra-carotid artery injection after MCAO. One possible mechanism of action was up-regulated antiapoptotic bcl-2, bcl-xl gene expression and down-regulated proapoptotic bax in the penumbra in the early stage of cerebral ischemia.
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