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作 者:黄敏丽[1] 罗国容[2] 陈维平[2] 何少健[2] 陈芳[2]
机构地区:[1]广西医科大学第一附属医院眼科,南宁530021 [2]广西医科大学组织胚胎学教研室,南宁530021
出 处:《眼科研究》2008年第6期448-450,共3页Chinese Ophthalmic Research
基 金:广西壮族自治区自然科学基金(桂科自0640090);广西壮族自治区教育厅博士研究生科研创新基金(2006105981001D13)资助
摘 要:目的模拟糖尿病视网膜病变(DR)的体内环境,观察血管形成抑制因子Tumstatin肽(T8肽)对高糖视网膜M櫣ller细胞条件培养基(HGMCM)诱导的视网膜脉络膜血管内皮细胞迁移的影响。方法采用细胞划痕实验,观察不同质量浓度的T8肽对HGMCM诱导的RF/6A细胞迁移的抑制作用。结果加入不同质量浓度的T8肽后,RF/6A细胞24 h、48 h迁移的距离显著降低,迁移距离随着T8肽质量浓度的增大而逐渐降低(P<0.01)。结论Tumstatin肽能够抑制HGMCM诱导的视网膜脉络膜血管内皮细胞迁移,可能是Tumstatin肽抗血管生成的机制之一。Objective Retinal neovascularization is one of the major pathological changes in diabetic retinopathy and involves migration and proliferation of retinal vascular endothelial cells. This study was to simulate the in vivo environment of diabetic retinopathy and evaluate the effect of tumstatin peptide(T8 peptide) on migration of retinochoroidal vascular endothelial cells cultured in high glucose Mfiller cell conditioned medium( HGMCM). Methods The third generation of Muller cells were cultured in 50 mmol/L D-glucose and free-serum RPMI 1640 for 48 hours to collect the Mfiller cell supernatant fluid. Cell line of retinochoroidal vascular endothelial cells of Macaca rhesus was inoculated in medium containing 15% FBS and Muller cell supernatant fluid and different concentrations of T8 peptide(0,5, 10,20 p,g/mL) was added in medium, namely TO, H + TO, H + T5, H + T10, H + T20 group respectively. Cultured RF/6A cells were scarificed by 200 μL Tip. Wound-healing assay was used to assess the effect of tumstatin on migration of RF/6A cells. Results Compared with that in TO group,the migration distance of RF/6A cells in cultured 24 hours and 48 hours were significantly longer in H + TO group(P 〈 0.01 ). After the cells treated with tumstatin for 24 hours and 48 hours ,the migration distance of RF/6A cells in H + TO was significantly longer than that in H + T5, H + T10 and H + T20 groups( P 〈 0. 01 ). The distances decreased gradually along with the increase of tumstatin concentration( P 〈 0.01 ). Conclusion Tumstatin can inhibit the migration of retinochoroidal vascular endothelial cells accelerated by HGMCM. This may be one of the mechanisms of tumstatin inhibiting angiogenesis.
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