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水蛭素对外伤性增生性玻璃体视网膜病变增殖膜抑制机制的探讨 被引量:9

The study of the mechanism of hirudin on inhibition of proliferative membranes in wounded proliferative vitreoretinopathy.
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摘要 目的 探讨水蛭素抑制外伤性增生性玻璃体视网膜病变 (proliferativevitreo retinopathy,PVR)增殖膜的作用及机理。方法 采用兔眼后段穿通伤制备的外伤性PVR模型 ,利用HE染色和免疫组化SP法结合图像分析半定量观察模型组、水蛭素组和生理盐水组玻璃体腔增殖膜的形态计量学、增殖细胞血小板源生长因子受体 -β (platelet-derivedgrowthfactorreceptor-β,PDGFR -β)积分光密度 (IOD)以及Ki67阳性细胞数的改变。用线性回归分析增殖膜面积与PDGFR -β、Ki67的量以及后两者之间的关系。结果 水蛭素组增殖膜的面积、周长、平均体积、体积密度、数密度低于观察模型组和生理盐水组 (P <0 0 5~ 0 0 1 ) ;水蛭素组Ki67阳性细胞数、PDGFR -βIOD明显低于观察模型组和生理盐水组 (P <0 0 5~ 0 0 1 )。模型组与生理盐水组之间以上指标差异无显著性 (P >0 0 5)。水蛭素组增殖膜面积与PDGFR -β、Ki67的量呈正直线相关 ,前者r=0 570 ,P <0 0 1 ,后者r=0 657,P <0 0 1 ;PDGFR -β与Ki67的量呈正直线相关r=0 71 9,P <0 0 0 1。结论 水蛭素能抑制增殖膜增殖细胞PDGFR的活化及降低其下游分子Ki67的产生 ,推测通过细胞外调节蛋白激酶 (extracellularregulatedproteinkinases,ERK)通路产生了抑制增殖细胞的? OBJECTIVE To study the action and mechanism of hirudin on inhibition of proliferative membranes of wounded proliferative vitreoretinopathy(PVR) METHODS The rabbit model of PVR was introduced by the penetrating injury at the posterior segment of an eyeball The hematoxylin and eosin staining, and the immunohistochemical SP methods combined with image analyses were used for semi-quantitative observation of the changes of norphometry of the proliferative membranes and integral optical density(IOD) of the platelet-derived growth factor receptor-β(PDGFR-β), and number of cell of the Ki67 protein of the proliferative cells in the observed model group, the hirudin group and the normal saline group The relation between area of the proliferative membranes and IOD of the PDGFR-β, and number of cell of the Ki67 and post-both each other analyzed with linear regression RESULTS The areas and the perimeters and the average volume and the volume density and the numerical density of the proliferative membranes reduced in the hirudin group vs the observed model group and the normal saline group ( P <0 05~0 01) The positive cell number of the Ki67 protein,the PDGFR- β IOD were lower in the hirudin group than the observed model group and the normal saline group ( P <0 05~0 01) There was not significant difference between the observed model group and the normal saline group( P >0 05) Relativity between the areas of the proliferative membranes and IOD of the PDGFR- β , and numbers of the Ki67 protein showed positive linear correlation( r =0 570, P <0 01, and r =0 719, P <0 001) CONCLUSION The hirudin could inhibit activation of the PDGFR of proliferative cells and reduce production of followed molecule-the Ki67 protein.It was presumed that effect of inhibition of the proliferative cells was by means of extracellular regulated protein kinases
出处 《中国中医眼科杂志》 2002年第4期187-191,共5页 China Journal of Chinese Ophthalmology
基金 四川省教委重点科研基金 (5 4 )
关键词 水蛭素 增生性玻璃体视网膜病变 免疫组织化学 血小板源生长因子受体-β KI67蛋白 hirudin proliferative vitreoretinopathy immunohistochemical platelet-derived growth factor receptor-β Ki67 protein
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