本文選題：未成熟兒視網(wǎng)膜病變 + 視網(wǎng)膜新生血管��； 參考：《青島大學(xué)》2010年碩士論文

【摘要】： 目的：通過建立氧誘導(dǎo)視網(wǎng)膜病變(OIR)小鼠模型模擬人類未成熟兒視網(wǎng)膜病變。予以PKC-β抑制劑Ruboxistaurin灌胃,檢測Ruboxistaurin對視網(wǎng)膜組織中VEGF表達(dá)的變化情況。 方法：建立氧誘導(dǎo)視網(wǎng)膜病變模型。隨機(jī)對120只7天齡C57BL/6J幼鼠分為正常對照組、高氧模型組、藥物治療組和空白對照組,除正常對照組外,其余幼鼠均暴露在濃度為(75±2)%的高氧狀態(tài)下5天,隨后正常氧環(huán)境下5天,建成氧誘導(dǎo)視網(wǎng)膜病變模型。藥物治療組和空白對照組又分別按照灌胃劑量的不同分為大,中,小劑量三個亞組。用免疫組織化學(xué)染色與逆轉(zhuǎn)錄—聚合酶鏈反應(yīng)法(RT-PCR)檢測視網(wǎng)膜組織中VEGF含量的變化。 結(jié)果：免疫組織化學(xué)染色顯示：正常對照組中,VEGF在視網(wǎng)膜組織中即有少量表達(dá)；高氧模型組中其表達(dá)水平升高,與正常對照組比較差異有統(tǒng)計學(xué)意義(P0.01), RT-PCR產(chǎn)物凝膠電泳檢測VEGFmRNA的含量與免疫組織化學(xué)結(jié)果一致。藥物治療組的三個亞組VEGF蛋白灰度值分別為132.7713±5.5100,138.0096±1.8700,143.2910±4.6600, VEGFmRNA相對表達(dá)量分別為0.8973±0.0600,0.8254±0.0400,0.6183±0.0300,正常對照組、高氧模型組,藥物治療組各組比較差異均具有統(tǒng)計學(xué)意義(P0.05),高氧模型組和空白對照組比較差異無統(tǒng)計學(xué)意義(P0.05) 結(jié)論：VEGF在氧誘導(dǎo)視網(wǎng)膜病變小鼠模型的視網(wǎng)膜中表達(dá)增強(qiáng)。OIR模型的視網(wǎng)膜組織中VEGF表達(dá)部分是通過PKC通路產(chǎn)生的。Ruboxistaurin可以減少OIR模型鼠視網(wǎng)膜組織中的VEGF的表達(dá)。
[Abstract]:Aim: to establish oxygen-induced retinopathy (OIR) mouse model to simulate human immature retinopathy. PKC- 尾 inhibitor Ruboxistaurin was administered intragastrically to detect the changes of VEGF expression in retina. Methods: oxygen-induced retinopathy model was established. 120 7-day-old C57BL/6J young rats were randomly divided into normal control group, hyperoxia model group, drug treatment group and blank control group. Except for normal control group, the other young rats were exposed to hyperoxia (75 鹵2%) for 5 days and then to normal oxygen environment for 5 days. Oxygen-induced retinopathy model was established. The drug treatment group and the blank control group were divided into three subgroups: large, middle and low dose according to the different dosage of gastric perfusion. Immunohistochemical staining and reverse transcriptase polymerase chain reaction (RT PCR) were used to detect the content of VEGF in retina. Results: immunohistochemical staining showed that there was a little expression of VEGF in the retina of the normal control group, but the expression level of VEGF in the hyperoxia model group was higher than that in the hyperoxia model group. Compared with the control group, the difference was statistically significant (P 0.01). The content of VEGFmRNA detected by gel electrophoresis of RT-PCR products was consistent with the results of immunohistochemistry. The gray values of VEGF protein in the three subgroups of the drug treatment group were 132.7713 鹵5.100 138.0096 鹵1.8700143.2910 鹵4.66000.The relative expression of VEGFmRNA was 0.8973 鹵0.0600,0.8254 鹵0.0400,0.6183 鹵0.0300, respectively. There was no significant difference between hyperoxia model group and blank control group (P 0.05). Conclusion the expression of VEGF in the retina of mice with oxygen-induced retinopathy is enhanced. The expression of VEGF in the retina of the mouse model of OIR induced retinopathy is partly induced by the PKC pathway. Ruboxistaurin can reduce the expression of VEGF in the retina of OIR model mice.
【學(xué)位授予單位】：青島大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2010
【分類號】：R774.1

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