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目的 探讨C fos原癌基因与先天性巨结肠症发病机制间的关系。方法 采用RT PCR技术及免疫组织化学SP方法对巨结肠无神经节细胞的巨结肠痉挛段以及有神经节细胞的扩张段、正常肠组织各 12例标本检测C fos原癌基因mRNA的表达和观察其蛋白免疫组化状况。结果 无神经节细胞的巨结肠痉挛段C fosmRNA表达水平明显高于有神经节细胞扩张段近端 (痉挛段相对含量 2 .11± 0 .0 9,扩张段相对含量 0 .5 5± 0 .0 6 ,单位 :mass) ,巨结肠扩张段近端与正常肠组织相比无明显差异 ;C fos蛋白免疫组化巨结肠无神经节细胞的痉挛段粘膜固有层和粘膜肌层中出现大量的棕褐色C fos蛋白表达产物 ,而巨结肠近段的扩张段未见C fos蛋白表达阳性产物。结论 C fos基因可能参与了神经细胞的损害。C fosmRNA表达及C fos蛋白表达异常可能参与先天性巨结肠的发病机制
Objective To investigate the relationship between C fos proto-oncogene and the pathogenesis of Hirschsprung’s disease. Methods The expression of C fos proto-oncogene mRNA was detected by RT-PCR and immunohistochemical SP method in 12 cases of megacolon spasticity without ganglion cell and in dilatation segment of normal ganglion cells and normal intestinal tissue Its protein immunohistochemistry. Results The expression of C fos mRNA in the ganglion cells without ganglion cells was significantly higher than that in the dilatation segments of ganglion cells (the relative content of spasticity was 2.11 ± 0.99, the relative content of dilatation was 0.55 ± 0. 0 6, unit: mass), there was no significant difference between the proximal part of megacolon expansion segment and normal intestinal tissue. There were a large number of mucosal lamina propria and muscularis mucosa in the spasm segment of H & Tan C fos protein expression products, while the expansion of the proximal part of megacolon no positive expression of C fos protein. Conclusion C fos gene may be involved in the damage of nerve cells. C fosmRNA expression and C fos protein expression may be involved in the pathogenesis of Hirschsprung’s disease