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目的观察缺氧时滋养层细胞细胞周期及凋亡变化。方法体外培养胎盘绒毛膜癌滋养层细胞株(BeWo细胞),二氯化钴(CoCl2)处理模拟化学缺氧。噻唑蓝法测定不同浓度(0、125、250、500μmol/L)CoCl2作用不同时相(6、12、24h)后细胞活力;流式细胞术检测250μmol/L CoCl2处理细胞不同时间(6、12、24h)后细胞周期和凋亡改变。结果 125μmol/L CoCl2对细胞活力无明显影响(P>0.05);250μmol/L CoCl2作用时细胞活力呈下降趋势(P>0.05);500μmol/L CoCl2处理6、12、24h后细胞活力均有明显下降(P<0.01)。250μmol/L CoCl2诱导构建滋养层细胞缺氧模型。250μmol/L CoCl2作用12、24h后,G2/M期细胞比例增多(分别为0.24±0.13和0.31±0.01)(P<0.05或P<0.01)。250μmol/L CoCl2作用细胞24h后细胞凋亡呈增加趋势(P>0.05)。结论成功构建了滋养层细胞体外缺氧培养模型。缺氧诱导滋养层细胞周期向G2/M期进展,增加细胞凋亡。
Objective To observe the cell cycle and apoptosis of trophoblast cells during hypoxia. Methods In vitro culture of human choriocarcinoma trophoblast cells (BeWo cells) and cobalt chloride (CoCl2) to simulate chemical hypoxia. The viability of cells treated with CoCl2 at different concentrations (0, 125, 250 and 500μmol / L) for different phases (6,12,24h) was determined by thiazolyl blue assay. Flow cytometry , 24h) after the cell cycle and apoptosis changed. Results 125μmol / L CoCl2 had no significant effect on cell viability (P> 0.05). The cell viability decreased when treated with 250μmol / L CoCl2 (P> 0.05). After 500μmol / L CoCl2 treatment for 6, 12 and 24 hours, Decreased (P <0.01). Induction of hypoxia in trophoblasts by 250μmol / L CoCl2. After treated with 250μmol / L CoCl2 for 12,24h, the proportion of cells in G2 / M phase increased (0.24 ± 0.13 and 0.31 ± 0.01 respectively) (P <0.05 or P <0.01). The apoptosis of cells treated with 250μmol / L CoCl2 for 24 hours showed an increasing trend (P> 0.05). Conclusion The in vitro hypoxia culture model of trophoblast cells was constructed successfully. Hypoxia induces the progression of trophoblast cell cycle to G2 / M phase and increases apoptosis.