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目的:利用RNA干扰技术,通过重组腺病毒导入,抑制脑组织中PARs基因的表达,观察神经功能缺陷评分、缺血脑组织梗死体积的变化,为缺血性脑血管疾病的基因治疗提供实验依据。方法:雄性Wistar大鼠随机分组,以重组腺病毒介导的无序PARs基因shRNA片段、生理盐水进行干预,干预3天后以线栓法建立Wistar大鼠大脑中动脉永久闭塞模型,各组分别于线栓后24h、72h进行神经功能缺陷评分并断头取脑,应用4%TTC染色测脑梗死体积。结果:1.缺血后24h、72h同一时间点:①实验组分别与对照组、生理盐水组对比,神经功能缺陷评分明显降低(P<0.05),脑梗死体积明显减小(P<0.05);②对照组与生理盐水组对比,神经功能缺陷评分、脑梗死体积无明显差异(P>0.05)。2.各组组内缺血后24h、72h对比,神经功能缺陷评分、脑梗死体积各组均有明显差异(P<0.05)。结论:重组腺病毒介导的RNAi能有效抑制脑组织中PARs基因的表达,缩小脑梗死体积,改善神经功能缺陷评分。
OBJECTIVE: To study the effect of recombinant adenovirus on the expression of PARs gene in brain tissue by RNAi technique. To observe the changes of neurological deficit score and infarct volume in ischemic brain tissue and to provide experimental basis for gene therapy of ischemic cerebrovascular disease . Methods: Male Wistar rats were randomly divided into three groups: the recombinant adenovirus-mediated PARs gene fragment and physiological saline intervention, and the permanent occlusion model of middle cerebral artery in Wistar rats was established by thread occlusion method. Neurological deficits were assessed at 24h and 72h after thread occlusion and the brain was decapitated. The infarct volume was measured by 4% TTC staining. At the same time points at 24 h and 72 h after ischemia: ①Compared with the control group and the saline group, the score of neurological deficit in the experimental group was significantly lower (P <0.05) and the volume of the cerebral infarction was significantly decreased (P <0.05) ; ②control group and saline group, neurological deficit score, cerebral infarction volume was no significant difference (P> 0.05). There was significant difference (P <0.05) between neurological deficit score and cerebral infarction volume in each group at 24h and 72h after ischemia. Conclusion: The recombinant adenovirus-mediated RNAi can effectively inhibit the expression of PARs gene in brain tissue, reduce the volume of cerebral infarction and improve the neurological deficit score.