【摘要】 目的研究细胞增殖、凋亡及其调节基因在慢性阻塞性肺病（ＣＯＰＤ）继发肺动脉高压中的作用。方法应用免疫组化及原位缺口末端ＤＮＡ碎片标记技术检测ＣＯＰＤ患者肺内细胞增殖及凋亡，并用Ｎｏｒｔｈｅｒｎ杂交检测ＣＯＰＤ患者肺内ｃｍｙｃ、ｂｃｌ２及ｐ５３基因表达。结果ＣＯＰＤ患者及对照组肺内（包括肺小血管壁）均存在着一定比率的增殖及凋亡细胞。两组相比，ＣＯＰＤ组增殖指数增高而凋亡指数减少，增殖与凋亡比值显著增高，约为对照组４倍。在ＣＯＰＤ患者肺内，增殖细胞绝大部分位于肺小血管壁，而凋亡细胞在肺小血管壁上较对照组少见。ｃｍｙｃ、ｂｃｌ２及蛋白表达在ＣＯＰＤ肺内比对照组明显增高，主要在肺小血管壁。ｃｍｙｃｍＲＮＡ表达量约为对照组３倍，ｂｃｌ２ｍＲＮＡ三条带表达量约为对照组２５～３５倍，ｐ５３基因ｍＲＮＡ表达量比对照组显著减少，约为１／３倍。结论可能由于ｃｍｙｃ、ｂｃｌ２及ｐ５３基因异常表达所致的细胞增殖与凋亡异常参与了ＣＯＰＤ时的肺血管结构改建的调节，亦即参与了ＣＯＰＤ继发的肺动脉高压过程更多还原

【Abstract】 Objective To study the roles of apoptosis and proliferation and relative genes expression in chronic obstructive pulmonary disease (COPD) and pulmonary hypertension. Methods Immunohistochemical technique was used for the detection of cell proliferation and expression of relative genes. In situ end labeling technique was used for the detection of nucleosomal DNA fragmentation of apoptotic cells, and Northern blot for the detection of expression of cmyc, bcl2 and p53 genes in the lungs with COPD. Results Both proliferative cells and apoptotic cells were found in the lungs with COPD or without COPD. In lung tissue with COPD. The proliferation index was increased significantly, whereas the apoptosis index was decreased significantly. Compared with controls, the ratio of proliferation to apoptosis in lungs with COPD was increased by 4 folds, and the expression of cmyc or bcl2 mRNA was significantly increased by 2.5～3 folds in lungs tissue with COPD. The expression of cmyc and bcl2 protein was also increased significantly in lungs with COPD, the two antigen were predominantly localized in small pulmonary vessels. The expression of p53 mRNA was significantly decreased by 3 folds in lung tissue with COPD. Conclusion The abnormality of apoptosis versus proliferation activities induced by cmyc, bcl2 and p53 genes may contribute to pulmonary vascular structural remodeling in COPD.更多还原