目的：观察活血散结中药复方含药血浆对血小板源性生长因子(platelet derived growth factor，PDGF)干预下兔RPE细胞增殖的影响。

方法：酶消化法获取RPE原代细胞，进行RPE细胞的原代培养和传代； 制备活血散结中药复方含药血浆； 选取第4代兔RPE细胞为实验细胞，PDGF低、中、高剂量(5、10、20μg/L)干预48h后，CCK-8法检测并选取适宜细胞实验干预浓度； 建立PDGF干预下RPE细胞增殖模型。实验分组为空白对照组(DMEM)、正常血浆组、PDGF(10μg/L)组、PDGF(10μg/L)+AG1296(10μmol/L)组、PDGF(10μg/L)+10%含药血浆组，PDGF(10μg/L)+20%含药血浆组，分别加入相应处理因素干预24h后，Transwell法测定兔RPE细胞迁移力； 而干预48h后，CCK-8法测定兔RPE细胞的细胞活力OD值。

结果：10%和20%浓度的活血散结中药复方含药血浆能有效抑制PDGF干预下RPE细胞的细胞活力、细胞迁移。

结论：活血散结中药复方含药血浆能够抑制PDGF干预下兔RPE细胞增殖，这可能是其有效治疗增殖性玻璃体视网膜病变的机制之一。

METHODS: Primary cells of RPE cells were obtained by enzymatic digestion, and the primitive culture and subculture of RPE cells were proceeded; prepared blood plasma-contained traditional Chinese medicine compound drug-containing plasma; the fourth genertation rabbit RPE cells were selected as the experimental cells by PDGF of low, medium and high doses(5μg/L, 10μg/L, 20μg/L)for 48h. Suitable concentration was detected and selected in cells experiment by using CCK-8 method. Establishing rabbit model of RPE cell proliferation treated with PDGF. The experimental groups were blank control group(DMEM), normal plasma group, PDGF(10 μg/L)group, PDGF(10 μg/L)+ AG1296(10 μmol/L)group, PDGF(10 μg/L)+ 10% drug-containing plasma, PDGF(10 μg/L)+ 20% drug-containing plasma. Respectively, transwell method was used to determine the migration of rabbit RPE cells after 24h intervention in each group; CCK-8 was used to determine the cell viability OD value of rabbit RPE cells after 48h of intervention in each group.

RESULTS: The plasma containing 10% and 20% concentration of invigorating blood and dissipating masses traditional Chinese medicine compound drug can effectively inhibit cell viability and cell migration of RPE cells treated with PDGF.

CONCLUSION: We found the certain concentration of invigorating blood and dissipating masses traditional Chinese medicine compound drug can effectively inhibit cell viability and cell migration of RPE cells treated with PDGF, which may be an effective treatment for proliferative vitreoretinopathy and provide a new way to study the mechanism of proliferative vitreoretinopathy.