Objective： The aim of this study was to investigate the growth inhibition effects and the mechanisms of trkA kinase inhibitor on human pterygium fibroblasts（HPF）. Methods： Three normal conjunctivas and eleven pter...Objective： The aim of this study was to investigate the growth inhibition effects and the mechanisms of trkA kinase inhibitor on human pterygium fibroblasts（HPF）. Methods： Three normal conjunctivas and eleven pterygiums were surgically collected, trkA and p75 was examined in different tissues by immunohistochemistry, trkA and p75 expression was detected in HPF by immumofluorescence method. After being treated with 10-80 nmol/L trkA kinase inhibitor for 24-96 h, the growth activities of HPF were studied by MTT colorimetry. Caspase-3 was inspected in HPF by spectrophotometric method. The apoptosis of HPF was detected by flow cytometry. Results： Expression of trkA and p75 was significantly observed in epithelium and fibroblast of pterygium tissues. Expression of trkAwas observed in epithelium and fibroblast of normal conjunc- tiva. Expression of p75 was only observed in epithelium of normal conjuncUva, trkA kinase inhibitor could effectively inhibit the growth of human pterygium fibroblasts in vitro in time and dose dependent manners. Caspase-3 expression was increased. The rates of apoptosis were 8.26%-29.62% （P 〈 0.01）. Conclusion： TrkA and p75 possibly participate in genesis and development of pterygium, trkA kinase inhibitor could induce apoptosis of human pterygium fibroblasts. Inducing apoptosis through changing the ratio of trkA and p75 in fibroblasts and up-regulate Caspase-3 was probably one of its molecular mechanisms.展开更多
文摘Objective： The aim of this study was to investigate the growth inhibition effects and the mechanisms of trkA kinase inhibitor on human pterygium fibroblasts（HPF）. Methods： Three normal conjunctivas and eleven pterygiums were surgically collected, trkA and p75 was examined in different tissues by immunohistochemistry, trkA and p75 expression was detected in HPF by immumofluorescence method. After being treated with 10-80 nmol/L trkA kinase inhibitor for 24-96 h, the growth activities of HPF were studied by MTT colorimetry. Caspase-3 was inspected in HPF by spectrophotometric method. The apoptosis of HPF was detected by flow cytometry. Results： Expression of trkA and p75 was significantly observed in epithelium and fibroblast of pterygium tissues. Expression of trkAwas observed in epithelium and fibroblast of normal conjunc- tiva. Expression of p75 was only observed in epithelium of normal conjuncUva, trkA kinase inhibitor could effectively inhibit the growth of human pterygium fibroblasts in vitro in time and dose dependent manners. Caspase-3 expression was increased. The rates of apoptosis were 8.26%-29.62% （P 〈 0.01）. Conclusion： TrkA and p75 possibly participate in genesis and development of pterygium, trkA kinase inhibitor could induce apoptosis of human pterygium fibroblasts. Inducing apoptosis through changing the ratio of trkA and p75 in fibroblasts and up-regulate Caspase-3 was probably one of its molecular mechanisms.
