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机构地区:[1]中国药科大学生命科学与技术学院,江苏南京210009
出 处:《药物生物技术》2008年第4期266-269,共4页Pharmaceutical Biotechnology
基 金:中国教育部博士点基金资助(No.20040316005)
摘 要:为研究重组水蛭素Ⅲ对半乳糖损伤的人晶状体上皮细胞(HLEC)的保护作用,采用D-半乳糖建立人晶状体上皮细胞损伤模型,用重组水蛭素Ⅲ作用于受损细胞,设置正常组、模型组、低、中和高剂量重组水蛭素Ⅲ组以及阳性药白内停组,观察各组细胞密度和形态,用MTT法检测各组细胞存活率,考察各组细胞内超氧化物歧化酶(SOD)活力。结果表明,当D-半乳糖浓度为50×10-3mol/L时,模型组与正常组细胞有显著差异。重组水蛭素Ⅲ作用后受损细胞的存活率和SOD活性显著提高。因此,重组水蛭素Ⅲ对半乳糖损伤的人晶状体上皮细胞有明显的保护作用。To investigate the protective effects of recombinant hirudin variant (rHV3) against injury in human lens epithelial cells (HLEC) induced by D-galactose, the damaged HLEC model was established, and different concentrations of rHV3 were used to repair the damaged cells. There were six experimental groups, normal group, model group, low level of rHV3 group, middle level of rHV3 group, high level of rHV3 group and pirenoxine group. The cells were observed under the phase-contrast microscope for any morphological changes, while the cell viability was assessed by methylthiazol tetrazolium (MTT) assay, and also superoxide dismutase (SOD) was analyzed. The results showed that there was significant difference between normal group and model group when the cells were under the condition of 50 × 10^-3mol/L. Cell viability and SOD activity increased significantly in rHV3 group when compared with model group. These results indicated that rHV3 could have the positive function in protecting the HLEC insulted by D-galactose.
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