摘要
目的：探讨oltipraz对人肺早期癌变是否有阻断作用及其作用的分子机制。方法：人胚肺组织培养，光镜病理检查、ELISA法分析GST-π蛋白含量，比色法测GSTs活性，免疫组化分析mP53基因表达。结果：病理分析显示oltipraz阻断人肺早期癌变在CSC运用前或同时运用效果较好；测GST-π含量CSC组为129．2±26．9，CSC／oltipraz组为80．3±12．7，DMSO组为79．5±15．5（ng／mgprotein），试验组与对照组差别明显（P＜0．05）；GSTs活性也有类似效果；组织mP53基因表达CSC组为阳性，DMSO组为阴性，CSC／oltipraz组多为弱阳性。结论：oltipraz对人肺早期癌变有较好的阻断作用，它能使GST-π、mP53基因表达减弱。
The inhibitory effect of oltipraz on cigarette smoking condensate (CSC) induced carcinogenesis and its possible molecular mechanism was studied in human fetal lung (HFL) tissue culture.Pathological examination and analysis revealed inhibition of HFL carcinogenesis prior to or at the same time CSC treatment was effective. Determination of GST-π protein content by ELISA revealed that it was 129.2 ±26.9ng/mg protein in CSC group: 80.3 ± 12.7ng/mg protein in CSC/oltipraz group,and 79.5±15.5ng/mg protein in DMSO group. There was obvious difference between test and control groups (P<0.05), and GSTs activity determined by colorimetry showed a similar trend.Finally, mP53 gene expression f studied by immunohistochemical assay, was positive in CSC group,weakly positive in CSC/oltipraz and negative in DMSO control. To conclude from above, oltipraz inhibited CSC-induced HFL carcinogenesis in early stage, and decreased GST-π and mP53 gene expression.
出处
《基础医学与临床》
CSCD
1999年第3期38-42,共5页
Basic and Clinical Medicine
