| 目的 体外培养正常人及白内障患者晶状体上皮细胞(lens epithelial cells,LECs)，分别检测bFGF在体外培养的正常人及白内障患者LECs中的表达，找出其表达规律及差异，以探讨bFGF在白内障患者的LECs中的作用。 方法 体外培养正常人及白内障患者LECs并传代；利用免疫组织化学法和免疫印迹法，检测bFGF在体外培养的正常人及白内障患者LECs不同阶段的蛋白水平的表达。 结果 原代培养的正常人及白内障患者LECs无明显差异，但在传代过程中白内障患者的LECs出现了较早的细胞老化现象；在正常人原代培养细胞和传代的LECs中检测不到bFGF的表达，或仅有微弱表达，而在白内障患者的原代培养细胞和传代的LECs中，bFGF的表达较正常组明显增多，并明确表达了分子量为17000的蛋白。 结论 动物的LECs较人类LECs有较高的增殖能力；bFGF在体外培养的正常人LECs中不论是原代还是继代都只有微弱表达或没有表达；bFGF在体外培养的白内障患者的LECs中表达增强，因为术后残留的晶状体上皮细胞引起损伤修复过程，合成并释放bFGF，造成晶状体上皮细胞的增殖、移行和纤维化，并可能成为后囊混浊的原因之一。
Objective To detect the expression of bFGF in LECs of normal person and cataract patients cultured in vitro respevtively. Found its expression regulation and difference, so as to investigate the role of bFGF in LECs of cararact patient. Methods LECs of normal and cataract persons were cultured in vitro. The expression of bFGF protein in LECs of normal person and cataract patients cultured in vitro at different passages were detectd by immunohistochemical staining and Western blots methods. Results There was no obvious morphological difference between the cells of primary passage from cataract patients and those from the normal person. Only two times later of passage, the LECs of cataract group appeared the change of aging contrasted with
normal group. We found there was no expression or only faint expression of bFGF in the primary passage or in subcultured passage. The expression of bFGF increased obviously in LECs of cataract patients than in normal group. The results showed that the bFGF protein of 17KD could be identified in LECs of cataract patient. Conclusions LECs of animal has better proliferation ability than those of human.There was no expression or only faint expression of bFGF in the primary passage or in subcultured passage of normal person cultured in vitro.The expression of bFGF increased obviously in LECs of cataract patients cultured in vitro. The remnants LECs of post-operation aroused damnification and rehabilitation course, in which bFGF was synthesized and released. The results of it induced the proliferation, metaplasia, and myofibroblast of LECs, so it may be one reason of posterior capsule opacification.
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