【摘要】：研究目的:通過局部應用VEGFR抑制劑PTK787,探討PTK787對骨缺損修復過程中血管再生相關因子的調(diào)節(jié)作用;同時探討血管再生的變化是否影響神經(jīng)再生。研究方法:取成年雄性大鼠32只隨機分成4組。在頂骨兩側(cè)對稱性的制備直徑為5mm的標準骨缺損模型,實驗組骨缺損區(qū)通過微型滲透泵以1ul/h的速度持續(xù)7天灌注PTK78713.125mg。對照組灌注液不含有PTK787的溶液。各組老鼠分別于術后3天、7天、14天、28天處死取材。通過對CD34、VEGF和VEGFR2進行免疫組化染色以及微血管計數(shù)評價PTK787對血管再生的影響。同時對不同時間點骨缺損區(qū)神經(jīng)元標記物βIII-tubulin進行免疫組織化學染色,探討PTK787調(diào)節(jié)血管再生過程中對神經(jīng)再生的影響。研究結(jié)果:結(jié)果表明骨缺損修復過程中各個時間點對照組CD34的表達均高于PTK787導入的實驗組,7天組及14天組實驗組與對照組CD34的陽性表達差異具有統(tǒng)計學意義(P0.05)。雖然實驗組與對照組血管數(shù)目的差異沒有統(tǒng)計學意義,但可以觀察到對照組血管數(shù)目均高于實驗組。VEGF的表達在7天、14天、28天組對照組高于實驗組,且7天、28天實驗組與對照組的差異具有統(tǒng)計學意義(P0.05)。VEGFR2的表達在3天,14天,28天對照組高于實驗組,且差異具有統(tǒng)計學意義(P0.05)。β-IIItublin在3天、7天、14天、28天實驗組的表達較對照組低,其中3天實驗組與對照組的差別具有統(tǒng)計學意義。結(jié)論:VEGFR抑制劑PTK787抑制骨修復過程中的血管再生,其可能是由于VEGF/VEGFR-2的表達降低而引起的。同時血管再生的抑制也對神經(jīng)再生產(chǎn)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.
【學位授予單位】：福建醫(yī)科大學
【學位級別】：碩士
【學位授予年份】：2015
【分類號】：R78

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