VEGFR抑制剂PTK787对骨修复过程中血管和神经再生的可能调节作用
发布时间：2018-08-02 19:38
【摘要】：研究目的:通过局部应用VEGFR抑制剂PTK787,探讨PTK787对骨缺损修复过程中血管再生相关因子的调节作用;同时探讨血管再生的变化是否影响神经再生。研究方法:取成年雄性大鼠32只随机分成4组。在顶骨两侧对称性的制备直径为5mm的标准骨缺损模型,实验组骨缺损区通过微型渗透泵以1ul/h的速度持续7天灌注PTK78713.125mg。对照组灌注液不含有PTK787的溶液。各组老鼠分别于术后3天、7天、14天、28天处死取材。通过对CD34、VEGF和VEGFR2进行免疫组化染色以及微血管计数评价PTK787对血管再生的影响。同时对不同时间点骨缺损区神经元标记物βIII-tubulin进行免疫组织化学染色,探讨PTK787调节血管再生过程中对神经再生的影响。研究结果:结果表明骨缺损修复过程中各个时间点对照组CD34的表达均高于PTK787导入的实验组,7天组及14天组实验组与对照组CD34的阳性表达差异具有统计学意义(P0.05)。虽然实验组与对照组血管数目的差异没有统计学意义,但可以观察到对照组血管数目均高于实验组。VEGF的表达在7天、14天、28天组对照组高于实验组,且7天、28天实验组与对照组的差异具有统计学意义(P0.05)。VEGFR2的表达在3天,14天,28天对照组高于实验组,且差异具有统计学意义(P0.05)。β-IIItublin在3天、7天、14天、28天实验组的表达较对照组低,其中3天实验组与对照组的差别具有统计学意义。结论:VEGFR抑制剂PTK787抑制骨修复过程中的血管再生,其可能是由于VEGF/VEGFR-2的表达降低而引起的。同时血管再生的抑制也对神经再生产生一定的抑制作用。
[Abstract]:Objective: to investigate the effects of VEGFR inhibitor PTK787 on the regulation of vascular regeneration related factors during bone defect repair and whether the changes of vascular regeneration affect nerve regeneration. Methods: 32 adult male rats were randomly divided into 4 groups. The standard bone defect model with the diameter of 5mm was prepared in the parietal bone symmetrically. In the experimental group, PTK 78713.125 mg / g was perfused to the bone defect area through a mini osmotic pump at the speed of 1ul/h for 7 days. The control group did not contain PTK787 solution. The rats in each group were killed 3 days, 7 days, 14 days and 28 days after operation. The effects of PTK787 on vascular regeneration were evaluated by immunohistochemical staining and microvessel count. At the same time, immunohistochemical staining of 尾 III-tubulin, a neuron marker in bone defect area at different time points, was carried out to investigate the effect of PTK787 on nerve regeneration in the process of vascular regeneration. Results: the results showed that the expression of CD34 in the control group was significantly higher than that in the experimental group on day 7 and day 14 during the bone defect repair (P0.05). Although there was no significant difference in the number of blood vessels between the experimental group and the control group, it was observed that the number of blood vessels in the control group was higher than that in the experimental group, and the expression of VEGF in the control group was higher than that in the control group on the 7th day and 14th day after 28 days. The expression of VEGFR2 in the experimental group was significantly higher than that in the control group on the 3rd day, the 14th day and the 28th day, and the difference was statistically significant (P0.05). The expression of 尾 -IIItublin in the experimental group was lower than that in the control group on the 3rd day, the 7th day, the 14th day, and the 28 day, the expression of VEGFR2 in the experimental group was lower than that in the control group. The difference between the experimental group and the control group was statistically significant on 3 days. Conclusion PTK787 inhibits vascular regeneration during bone repair, which may be due to the decrease of VEGF/VEGFR-2 expression. At the same time, the inhibition of vascular regeneration also has a certain inhibitory effect on nerve regeneration.
【学位授予单位】：福建医科大学
【学位级别】：硕士
【学位授予年份】：2015
【分类号】：R78
[Abstract]:Objective: to investigate the effects of VEGFR inhibitor PTK787 on the regulation of vascular regeneration related factors during bone defect repair and whether the changes of vascular regeneration affect nerve regeneration. Methods: 32 adult male rats were randomly divided into 4 groups. The standard bone defect model with the diameter of 5mm was prepared in the parietal bone symmetrically. In the experimental group, PTK 78713.125 mg / g was perfused to the bone defect area through a mini osmotic pump at the speed of 1ul/h for 7 days. The control group did not contain PTK787 solution. The rats in each group were killed 3 days, 7 days, 14 days and 28 days after operation. The effects of PTK787 on vascular regeneration were evaluated by immunohistochemical staining and microvessel count. At the same time, immunohistochemical staining of 尾 III-tubulin, a neuron marker in bone defect area at different time points, was carried out to investigate the effect of PTK787 on nerve regeneration in the process of vascular regeneration. Results: the results showed that the expression of CD34 in the control group was significantly higher than that in the experimental group on day 7 and day 14 during the bone defect repair (P0.05). Although there was no significant difference in the number of blood vessels between the experimental group and the control group, it was observed that the number of blood vessels in the control group was higher than that in the experimental group, and the expression of VEGF in the control group was higher than that in the control group on the 7th day and 14th day after 28 days. The expression of VEGFR2 in the experimental group was significantly higher than that in the control group on the 3rd day, the 14th day and the 28th day, and the difference was statistically significant (P0.05). The expression of 尾 -IIItublin in the experimental group was lower than that in the control group on the 3rd day, the 7th day, the 14th day, and the 28 day, the expression of VEGFR2 in the experimental group was lower than that in the control group. The difference between the experimental group and the control group was statistically significant on 3 days. Conclusion PTK787 inhibits vascular regeneration during bone repair, which may be due to the decrease of VEGF/VEGFR-2 expression. At the same time, the inhibition of vascular regeneration also has a certain inhibitory effect on nerve regeneration.
【学位授予单位】：福建医科大学
【学位级别】：硕士
【学位授予年份】：2015
【分类号】：R78
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