摘要
目的研究重组人促红细胞生成素（rhEPO）对光损伤诱导的人视网膜色素上皮（RPE）细胞Bcl-2表达的影响及其作用机制。方法取成人ARPE-19细胞株传代培养的2-5代细胞建立光损伤模型,采用酶联免疫吸附实验和免疫组织化学方法检测不同浓度rhEPO干预治疗前后RPE细胞Bcl-2表达的变化;并添加特异性Jak2激酶抑制剂AG490,检测RPE细胞Bcl-2表达的变化。结果 rhEPO可明显增强RPE细胞光损伤后Bcl-2的表达,与光损伤模型组相比较,rhEPO各药物干预组细胞Bcl-2表达均增强,差异有显著意义（F=18.756,q=36.028~44.285,P〈0.01）,以40 kU/L rhEPO组作用最明显。而加入AG490后,rhEPO对Bcl-2的上调作用被明显阻断（q=42.171,P〈0.01）。结论 rhEPO可能是通过增强Bcl-2的表达而抑制光损伤诱导的人RPE细胞的凋亡,rhEPO上调Bcl-2的表达可能是通过Jak2 PIK3/PKB途径实现的。
Objective To study the effect of recombinant human erythropoietin（rhEPO） on expression of Bcl-2 in light-injured human retinal pigment epithelial（RPE） cells,and explore its mechanism against apoptosis.Methods Human ARPE-19 cell strain at passages 2-5 was harvested to create a light-injured model.The light-injured human RPE cells were treated with different doses of rhEPO,and thereafter with the specific inhibitors of Jak2（AG490）.The expression of Bcl-2 in light-injured human RPE cells with different treatment was assessed by enzyme linked immunosorbant assay and immunohistochemistry.Results The expression of Bcl-2 in light-injured human RPE cells in each rhEPO group was obviously increased,compared with that in model group（F=18.756;q=36.028-44.285;P0.01）.The most conspicuous increase observed in the group with 40 kU/L rhEPO.With adding of AG490,up-regulation of expression of Bcl-2 by rhEPO was significantly inhibited（q=42.171,P0.01）.Conclusion rhEPO inhibits the apoptosis of light-injured human RPE cells is probably by enhancing the expression of Bcl-2,while the up-regulation of Bcl-2 by rhEPO is likely achieved via the Jak2-PIK3/PKB pathway.
出处
《青岛大学医学院学报》
CAS
2011年第3期194-196,共3页
Acta Academiae Medicinae Qingdao Universitatis
基金
国家自然科学基金资助项目(30572010)
