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背景:氟桂嗪和转化生长因子β(TGF-β)都具有抗脑缺血损伤作用,但两者之间是否存在某种联系,目前还不明确。目的:通过研究氟桂嗪对沙鼠脑缺血再灌注后脑内转化生长因子I型,II型受体(TβRI,II)基因表达的影响,探讨氟桂嗪与TGFβ信号转导途径在抗脑缺血损伤方面的联系。设计:随机对照的实验研究。地点和对象:实验在中南大学湘雅二医院中心实验室完成。健康雄性蒙古沙鼠60只,9月龄,体质量(90±5)g,随机分为脑缺血组、氟桂嗪治疗组、假手术组、正常对照组,其中脑缺血组、氟桂嗪治疗组各有缺血再灌6h,1,3,7d组,共计10组,每组6只。干预:夹闭双侧颈总动脉法制作沙鼠脑缺血再灌注模型,氟桂嗪治疗组实验前1d给沙鼠喂食氟桂嗪犤按20mg/(kg·d)犦。采用原位杂交检测TβRI,II基因表达情况,用苏木精-伊红染色方法观察脑组织病理变化。主要观察指标:脑组织病理变化,及脑内TβRI,IImRNAs的表达。结果:氟桂嗪治疗组在再灌注各个时间点脑组织损伤程度均明显轻于脑缺血组。各组沙鼠脑组织的神经元和胶质细胞胞浆均有TβRI,IImRNAs阳性表达。棕褐色颗粒主要位于神经元和胶质细胞胞浆中,但表达程度有所不同。假手术组的TβRI,IImRNAs的表达较正常对照组稍高但无明显差异(P>0.05)。氟桂嗪治疗组中缺血再灌注6h,1d,3dTβRI,IIm
BACKGROUND: Both flunarizine and transforming growth factor-β (TGF-β) have anti-ischemic effects. However, it is unclear whether there is any correlation between the two. OBJECTIVE: To investigate the effect of flunarizine on the gene expression of transforming growth factor type I and type II receptor (TβRI, II) in gerbiled rat brain after cerebral ischemia and reperfusion, and to explore the effect of flunarizine and TGFβ signaling pathway on anti- Ischemic injury connection. Design: Randomized controlled experimental study. Location and object: The experiment was completed at the Central Laboratory of Xiangya Second Hospital of Central South University. Sixty healthy male Mongolian gerbils, aged 9 months old, weighing 90 ± 5 g, were randomly divided into cerebral ischemia group, flunarizine treatment group, sham operation group and normal control group. The cerebral ischemia group, The cinnamidine group had 6h, 1,3,7d ischemia and reperfusion groups, respectively, a total of 10 groups, 6 in each group. Intervention: The model of gerbil cerebral ischemia / reperfusion was established by occluding both common carotid arteries. Flunarizine was fed to gerbils by 20mg / (kg · d) 1 1d before flunarizine treatment. The expression of TβRI and II genes was detected by in situ hybridization. The pathological changes of brain tissue were observed by hematoxylin-eosin staining. MAIN OUTCOME MEASURES: Pathological changes of brain tissue, and expressions of TβRI and II mRNA in the brain. Results: The flunarizine treatment group at each time point of reperfusion brain injury were significantly lighter than the cerebral ischemia group. T neurons and glial cytoplasm in each group of gerbil brain tissue TβRI, IImRNAs positive expression. Tan particles are mainly located in the cytoplasm of neurons and glial cells, but the degree of expression is different. The expression of TβRI and II mRNA in the sham operation group was slightly higher than that in the normal control group (P> 0.05). Flunarizine treatment group ischemia-reperfusion 6h, 1d, 3dTβRI, IIm