摘要
目的：探讨无氧和／或低氧（０％Ｏ２和／或２５％Ｏ２）对肺动脉内皮细胞（ＰＡＥＣ）活力和增殖的影响。方法：应用形态学观察、细胞活力测定、流式细胞技术、３Ｈ－ＴｄＲ掺入、免疫组化染色等方法。结果：缺氧使ＰＡＥＣ胞浆内的线粒体和粗面内质网增多，随缺氧时间的延长，线粒体肿胀、空泡化，内质网扩张。ＭＴＴ法细胞活力测定显示无氧６ｈ末ＰＡＥＣ的细胞活力无明显变化，无氧１２ｈ至２４ｈ末ＰＡＥＣ的细胞活力明显增加（Ｐ＜００１）。在６ｈ，１２ｈ，１８ｈ，２４ｈ，低氧和无氧使ＰＡＥＣ的３Ｈ－ＴｄＲ掺入显著少于常氧对照组（Ｐ＜００５）。无氧２４ｈ末ＰＡＥＣ的增殖细胞核抗原（ＰＣＮＡ）阳性反应颗粒明显少于常氧对照组，且常氧组ＰＣＮＡ含量是无氧组的３７５倍。然而流式细胞分析显示，与常氧对照组相比，无氧和低氧ＰＡＥＣ的Ｓ期和Ｇ２／Ｍ期细胞比例明显增多（Ｐ＜００１）、Ｇ０／Ｇ１期细胞比例明显减少（Ｐ＜０．００１），细胞内总蛋白除无氧１２ｈ组外含量均显著增多（Ｐ＜０．００１）。结论：缺氧可激活ＰＡＥＣ使其细胞活力增加，但却抑制其增殖；缺氧ＰＡＥＣ的Ｇ２／Ｍ期细胞增多，可能由于缺氧通过延长细胞周期时间和使ＰＡＥＣ的Ｇ２／Ｍ期细胞和Ｇ?
Abstract AIM:To investigate the effects of hypoxia (2.5%O 2 and/or 0%O 2) on bovine pulmonary artery endothelial cells (PAEC) proliferation and cell viability.METHODS:Cell proliferation and viability were determined using 3H-thymidine incorporation and flow cytometry analysis and MTT colorimetric assay. RESULTS:Hypoxic endothelial cells were characterised by large increase in endoplasmic reticulum and mitochondria, then the endoplasmic reticulum became dilated, the mitochondria became swollen, when hypoxic exposure lengthened. PAEC cell viability unchanged at the end of 6h anoxia and then increased significantly from 12h to 24h anoxia ( P <0.01). Hypoxia and anoxia significantly attenuated 3H-thymidime incorporation by PAEC at 6h to 12h exposure ( P <0 05). Flow cytometric DNA analysis revealed that hypoxia induced significantly enhancement of S phase and G 2/M phase and decreaced G 0/G 2 phase ( P <0 001). Immunocytochemical reaction of proliferating cell nuclear antigen (PCNA) of PAEC under normoxic condition was more stronger than that of anoxic PAEC at 24h, the PCNA content of normoxic PAEC was 3.75 times more than that of anoxic PAEC. CONCLUSION:Hypoxia may stimulate PAEC cell viability, but inhibit proliferation of PAEC, which may involve in regulating the development of hypoxic pulmonary hypertension and angiogenesis. MeSH Anoxia; Pulmonary artery; Endothelium; Cell survival
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
1998年第6期583-587,共5页
Chinese Journal of Pathophysiology
基金
国家自然科学基金
