受体蛋白质酪氨酸激酶抑制剂影响兔晶状体上皮细胞增生的研究

目的　研究受体蛋白质酪氨酸激酶 (receptorprotein tyrosinekinase,RPTK)抑制剂染料木黄酮对兔晶状体上皮细胞增生和胞膜RTPK活性的影响 ,探讨使用染料木黄酮防治后发性白内障发生的机制。方法　培养兔晶状体上皮细胞 ;测定 5、10和 15mg/L染料木黄酮作用晶状体上皮细胞 3d的氚标记胸腺嘧啶脱氧核苷 (tritiatdethymidine,3 H TdR)掺入率 ,以无染料木黄酮作用的晶状体上皮细胞作为对照组 ;应用Casnetllie改良法检测不同浓度染料木黄酮作用 2 4h后 ,兔晶状体上皮细胞膜RTPK活性的变化。结果　 5、10和 15mg/L染料木黄酮作用晶状体上皮细胞 3d的3 H TdR掺入率分别为 6 30± 137、4 89± 16 6和 314± 98,与对照组比较差异均有显著意义 (P <0 0 5 ) ,且细胞增生抑制率随浓度增加而升高 ;不同浓度染料木黄酮作用 2 4h后兔晶状体上皮细胞中RTPK的活性均明显下降 ,其中 10和 15mg/L染料木黄酮作用的晶状体上皮细胞RTPK单位活性与无染料木黄酮作用者比较 ,差异均有显著意义 (P <0 0 5 )。结论　染料木黄酮在体外可通过抑制细胞膜RTPK的活性而抑制兔晶状体上皮细胞增生

Effect of genistein on proliferation of rabbit lens epithelial cell

OBJECTIVE: To assess the effects of genistein (inhibitor of receptor protein-tyrosine kinase) on the proliferation of rabbit lens epithelial cells (RLEC) and the activity of cell membrane receptor protein-tyrosine kinase (RTPK) of RLEC and approach the mechanism of genistein in prevention and treatment of after cataract. METHODS: RLECs were cultured in vitro with the addition of 0 (control), 5, 10 and 15 mg/L genistein. The proliferation rates of the cells were measured by tritiated thymidine ((3)H-TdR) incorporation, and Casnetllie modified method was used to measure RTPK activities on the cell membrane after the action of various concentrations of genistein maintaining for 24 hours. RESULTS: The rates of (3)H-TdR incorporation in the cultures with 5, 10 and 15 mg/L genistein for 3 days were 630 +/- 137, 489 +/- 166 and 314 +/- 98, respectively. The rates were all different from the rate of the control significantly (P < 0.05), and the inhibition rate of cell proliferation was elevated along with the increase of the genistein concentration. After the maintenance of the action of genistein for 24 hours, the activity of RTPK was significantly lowered in the RLECs. The activity in the culture with 10 and 15 mg/L was significantly different from that in the control (P < 0.05). CONCLUSION: In vitro, genistein may inhibit the proliferation of RLECs via the inhibition of the activity of the cell membrane RTPK.