摘要
目的和方法:应用免疫组织化学、原位末端标记技术及Northern杂交等方法检测慢性缺氧大鼠肺内特别是肺血管壁细胞增殖、凋亡及相关基因cmyc、p53表达。结果:正常及慢性缺氧大鼠肺内检出一定比率的增殖、凋亡阳性细胞,两类细胞在肺内呈不均匀散在分布。在缺氧大鼠肺内,增殖阳性细胞绝大部分是肺小血管壁细胞,凋亡性染色细胞在肺小血管壁上较对照组少见。缺氧1、2周组大鼠肺内细胞增殖指数显著增高而凋亡指数显著减少,细胞增殖凋亡比值分别约为对照组3与35倍。cmyc及p53是细胞增殖、凋亡密切相关的两种癌(抑癌)基因,前者在缺氧大鼠肺内表达显著增加,而后者(野生型)表达显著减少。结论:可能由于cmyc及p53基因异常表达所致的细胞增殖、凋亡失衡参与了慢性缺氧性肺血管结构改建的调节。
Aim and Methods:By use of immunohistochemical technique, in situ terminal transferase labeling and Northern blot, the present study investingated cell proliferation, apoptosis and expression of c myc and p53 genes in lungs especially pulmonary vessels of rats exposed to chronic hypoxia.Results: Cell proliferation and apoptosis were all found in lungs of rats exposed to chronic hypoxia for one week or two weeks and of controls. In lungs of two hypoxic groups,proliferative cells mainly localized in small pulmonary vessels, but apoptotic cells were less in pulmonary vessels.Compared with controls, the proliferation index was significantly increased in lungs of two hypoxic groups,but the apoptotic index was significantly decreased.The ratio of proliferaation to apoptosis in lungs of two hypoxic groups was increased by 3 and 3.5 folds.c myc and p53 genes are very relative to cell proliferation and apoptosis.We found that the expression of c myc in lungs of two hypoxic groups was increased significantly,but the expression of p53 was decreased significantly.Conclusion: The misbalance btween proliferation and apoptosis which might be relative to abnormal expression of c myc and p53 minght contribute to pulmonary vascular structural remodeling.
出处
《中国应用生理学杂志》
CAS
CSCD
1999年第2期169-172,共4页
Chinese Journal of Applied Physiology