本文關(guān)鍵詞： 基質(zhì)金屬蛋白酶-2 基質(zhì)金屬蛋白酶-9 基質(zhì)金屬蛋白酶抑制劑-1 基質(zhì)金屬蛋白酶抑制劑-2 GM6001 外傷性增生性玻璃體視網(wǎng)膜病變 免疫組化 逆轉(zhuǎn)錄聚合酶鏈反應(yīng)　出處：《福建醫(yī)科大學(xué)》2007年碩士論文　論文類型：學(xué)位論文

【摘要】： 目的:觀察外傷性PVR和外傷后應(yīng)用GM6001大鼠視網(wǎng)膜組織MMP-2、MMP-9及TIMP-1、TIMP-2在不同病程中的表達(dá)變化,以期探討MMP-2、MMP-9及TIMP-1、TIMP-2在PVR形成過(guò)程中的作用,評(píng)價(jià)GM6001防治外傷性PVR的效果。 方法:360只SD大鼠隨機(jī)分為正常對(duì)照組、外傷性PVR組和外傷后應(yīng)用GM6001組。正常對(duì)照組玻璃體腔內(nèi)注射生理鹽水;外傷性PVR組玻璃體腔內(nèi)注射PRP血漿制成外傷性PVR大鼠動(dòng)物模型;外傷后應(yīng)用GM6001組在外傷后12h玻璃體腔內(nèi)注射GM6001。應(yīng)用免疫組化染色方法和逆轉(zhuǎn)錄聚合酶鏈反應(yīng)(RT-PCR)法分別于1、3、7、14、21、28d對(duì)各組大鼠視網(wǎng)膜組織MMP-2、MMP-9及TIMP-1、TIMP-2的表達(dá)進(jìn)行定性、定位、半定量檢測(cè)。 結(jié)果: 1、免疫組化結(jié)果示MMP-2、MMP-9、TIMP-1、TIMP-2蛋白均主要表達(dá)于視錐視桿層、視網(wǎng)膜內(nèi)外網(wǎng)狀層、神經(jīng)纖維層。 2、MMP-2、MMP-9在正常對(duì)照組、外傷后應(yīng)用GM6001組的各個(gè)亞組微弱表達(dá)。MMP-9在外傷性PVR組137d顯著表達(dá),與正常對(duì)照組和外傷后應(yīng)用GM6001組的差異有顯著性(P㩳0.01),隨著病程的延長(zhǎng),MMP-9的表達(dá)呈進(jìn)行性減弱的趨勢(shì);MMP-2在外傷性PVR組142128d表達(dá)增強(qiáng),與正常對(duì)照組和外傷后應(yīng)用GM6001組的差異有顯著性(P㩳0.01),隨著病程的延長(zhǎng),MMP-2的表達(dá)呈進(jìn)行性增高的趨勢(shì)。TIMP-1、TIMP-2在外傷性PVR組與外傷后應(yīng)用GM6001組的各個(gè)亞組均有明顯表達(dá),與正常對(duì)照組的差異均有顯著性(P㩳0.01)。 3、MMP-9/TIMP-1比率在外傷性PVR組137d增高,與正常對(duì)照組和外傷后應(yīng)用GM6001組的差異有顯著性(均P㩳0.05);MMP-2/TIMP-2比率外傷性PVR組142128d增高,與正常對(duì)照組和外傷后應(yīng)用GM6001組的差異有顯著性(均P㩳0.05)。 4、RT-PCR結(jié)果示MMP-2、MMP-9、TIMP-1、TIMP-2mRNA以及MMP-2/TIMP-2和MMP-9/TIMP-1的比率與免疫組織化學(xué)結(jié)果相平行。 結(jié)論: MMP-2、MMP-9、TIMP-2、TIMP-1參與了PVR發(fā)生發(fā)展的病理過(guò)程,MMP-2"TIMP-2、MMP-9"TIMP-1比率增高促進(jìn)PVR發(fā)生發(fā)展的進(jìn)程。人工合成基質(zhì)金屬蛋白酶抑制劑GM6001可促進(jìn)MMP-2"TIMP-2、MMP-9"TIMP-1動(dòng)態(tài)平衡的重新建立,從而在外傷性PVR的防治中起重要作用。
[Abstract]:Objective: to observe the changes of MMP-2MMP-9 and TIMP-1 TIMP-2 expression in retina of traumatic PVR and post-traumatic GM6001 rats. The purpose of this study was to investigate the role of MMP-2, MMP-9 and TIMP-1 and TIMP-2 in the formation of PVR, and to evaluate the effect of GM6001 on the prevention and treatment of traumatic PVR. Methods Twenty six hundred and thirty six Sprague-Dawley rats were randomly divided into three groups: normal control group, traumatic PVR group and post-traumatic GM6001 group. Traumatic PVR rat model was established by intravitreal injection of PRP plasma into the vitreous cavity of traumatic PVR group. GM6001 was injected into the vitreous cavity 12 hours after injury in GM6001 group. Immunohistochemical staining and reverse transcriptase polymerase chain reaction (RT-PCR) were used to detect GM6001. The expression of MMP-2MMP-9 and TIMP-1 TIMP-2 in the retina of rats in each group were detected qualitatively, locally and semi-quantitatively. Results: 1. The results of immunohistochemistry showed that MMP-2, MMP-9, TIMP-1and TIMP-2 were mainly expressed in the optic cone layer, the inner and outer retina reticular layer, and the nerve fiber layer. (2) MMP-2MMP-9 was expressed weakly in the normal control group and each subgroup of the GM6001 group after trauma. MMP-9 was expressed in the traumatic PVR group 1? 3? After 7 days, there was a significant difference in the expression of GM6001 between the normal control group and the post-traumatic GM6001 group. The expression of MMP-9 was gradually decreased with the prolongation of the course of disease. The expression of MMP-2 in traumatic PVR group was 14? 21? After 28 days, the expression of GM6001 was significantly higher than that of normal control group and post-traumatic GM6001 group. The expression of MMP-2 increased gradually with the prolongation of the course of disease. The expression of TIMP-2 in all subgroups of traumatic PVR group and post-traumatic GM6001 group was significantly higher than that in normal control group. 0.01g. 3The ratio of MMP-9 / TIMP-1 in traumatic PVR group was 1? 3? After 7 days, there was a significant difference between normal control group and post-traumatic GM6001 group (P < 0.05). The ratio of 0. 05% MMP-2 / TIMP-2 in traumatic PVR group was 14? 21? After 28 days, there was a significant difference between normal control group and post-traumatic GM6001 group (P < 0.05). 0.05. 4 the results of RT-PCR showed that MMP-2, MMP-9 and TIMP-1. The ratios of TIMP-2mRNA, MMP-2/TIMP-2 and MMP-9/TIMP-1 were parallel to those of immunohistochemistry. Conclusion: MMP-2, MMP-9, TIMP-2 and TIMP-1 are involved in the pathogenesis and development of PVR with MMP-2 "TIMP-2." The increase of MMP-9 "TIMP-1 ratio promotes the development of PVR. Synthetic matrix metalloproteinase inhibitor GM6001 can promote MMP-2" TIMP-2. The establishment of dynamic balance of MMP-9 "TIMP-1" plays an important role in the prevention and treatment of traumatic PVR.
【學(xué)位授予單位】：福建醫(yī)科大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2007
【分類號(hào)】：R779.1

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相關(guān)期刊論文 前1條

1 賈洪真,韓泉洪,惠延年,王琳,杜紅俊,崔志利,馬吉獻(xiàn);單核細(xì)胞趨化蛋白-1和基質(zhì)金屬蛋白酶-2在增生性玻璃體視網(wǎng)膜病變?cè)錾ぶ械谋磉_(dá)[J];眼科新進(jìn)展;2003年05期

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本文編號(hào)：1466002