【摘要】 应用原位杂交、免疫细胞化学及免疫斑点法观测香烟烟雾提取物 ( CSE)和酪氨酸激酶抑制剂 tyrphostin2 5作用后 ,培养的猪气道上皮细胞上皮钙粘附素 ( E- cd) m RNA和蛋白、增殖细胞核抗原 ( PCNA)的表达及培养上清液中可溶型 E- cd( s E- cd)含量的变化。结果发现 ,加入 CSE作用 4 h后 ,C4组细胞内 E- cd表达比对照 N4组降低了 3 6%( P<0 .0 1) ,而 2 4 h后 ,C2 4组 E- cd表达为对照 N2 4组的 1.72倍 ( P<0 .0 1)。PCNA表达量 C2 4组细胞为 N2 4组的1.3 8倍 ( P<0 .0 1) ,而加入 tyrphostin2 5和 CSE作用 2 4 h后 ,CT2 4组细胞比 N2 4组降低了 4 0 % ( P<0 .0 1)。培养上清液中 s E- cd的含量 C4组和 CT2 4组分别为相应 N组的 1.3 4倍和 2 .0 2倍 ,C2 4组比 N2 4组降低了 14 %。结果表明 :酪氨酸激酶活化时 ,E- cd滞留在胞浆中 ,细胞增殖能力增强 ;酪氨酸激酶活性抑制时 ,E- cd稳定表达于膜上 ,细胞增殖能力减弱。培养上清液中 s E- cd的含量可间接反映气道上皮细胞损伤修复的状态。更多还原

【Abstract】 The changes in the expression of E-cadherin (E-cd ) mRNA and protein, proliferative cell nuclear antigen (PCNA) in the medium of cultured porcine airway epithelial cells and soluble E-cd (sE-cd) content in the supernatant were measured by using in situ hybridization, immunocytochemistry and immunoblot analysis after incubation of cigarette smoke extract (CSE) with tyrosine kinase inhibitor tyrphostin 25. The results showed that after the 4 h incubation with CSE, the E-cd expression in the group C4 was decreased by 36 % as compared with that in the control group N4 (P<0 01); After the 24 h-incubation, the E-cd expression in the group C24 was 1 72-fold in comparison with the control group N24 (P<0 01). The PCNA expression in the group C24 was 1.38-fold in comparison with group N24 (P<0 01). After the 24 h incubation with tyrphostin25 and CSE, the PCNA expression in the group CT24 was reduced by 40 % as compared with that in the group N24 (P<0 01). The sE-cd content in the medium in the group C4 was 1 34-fold in comparison with group N4, the sE-cd content in the medium in the groups C24 and CT24 was reduced by 14 % and 2 02-fold as compared with group N24 respectively. It was suggested that when the tyrosine kinase was activated, E-cd was retarded in the cytoplasm with increased proliferation, as the tyrosine kinase was inhibited, E-cd was stable on the membrane with decrease proliferation. The sE-cd content in medium may indirectly indicate the state of injury and repair of airway epithelial cells.更多还原