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作 者:王虎[1] 于雪艳[2] 张士国[3] 胡国强[4] 任贵杰[2] 田克力[2]
机构地区:[1]中国医学科学院中国协和医科大学阜外心血管病医院中德分子医学研究室,北京市100037 [2]山东大学西校区生化教研室,济南市2250012 [3]济南军区总医院检验科,济南市3250014 [4]山东大学齐鲁医院胸外科,济南市4250012
出 处:《中国分子心脏病学杂志》2004年第4期228-232,共5页Molecular Cardiology of China
基 金:国家自然科学基金资助项目 (39770 730 )
摘 要:目的 观察 9 cis RA对肺腺癌细胞株PG和A5 49生长抑制、诱导分化和凋亡的作用。方法 将两株细胞分为 1μM、 5 μM 9 cis RA组和对照组 ,应用细胞计数方法统计每组各时相细胞数 ,苏木精—伊红染色观察细胞分化情况 ,流式细胞仪分析检测细胞凋亡。结果 (1)加入 9 cis RA 12h后 ,PG细胞生长受抑程度显著高于对照组 (p <0 0 1) ,且 5 μM组较 1μM组受抑程度更高 ,而A54 9细胞变化不明显。 (2 )加入 9 cis RA 2 4h后观察到PG细胞出现明显的分化特征 ,A54 9分化征象不明显 ,仅见分裂象减少。 (3)加入 9 cis RA 2 4h后PG细胞 1μM组和 5 μM组凋亡率均显著高于对照组 (p <0 0 1) ,且5 μM组凋亡率亦明显高于 1μM组 (p <0 0 1) ,A54 9细胞 5 μM组凋亡率明显高于对照组 (p <0 0 1) ,而1μM组与对照组无显著性差异。结论 9 cis RA对PG细胞株有明显的生长抑制、诱导分化和凋亡的作用 ,而对A54 9细胞的作用较弱 ,表明不同的细胞株对 9 cis RA的敏感性存在差异。Objective To observe the effects of 9-cis-RA on growth inhibition, differentiation and apoptosis induction in PG and A549 humanlung glandular cancer cells. Methods Dividing PG and A549 lung glandular cancer cells each into three groups: 1μm 9-cis-RA group, 5μM group and control group. Cell numbers of each group in different time-phases was by cell count methods. Apoptosis was detected by flow cytometric cell cycle analysis. Results (1) Form 12h after being treated with 9-cis-RA, the growth of PG cell was inhibited significantly, especially in 5μM group, but A549 cell has no distinct change. (2)After being treated with 9-cis-RA, features of cell differentiation were distinct in PG cell. A549 cell has no change. (3)From 24h after being treated with 9-cis-RA, the percentages of apoptotic cells were higher significantly in PG cell (p 〈 0.01), compared with control group. And the percentages of apoptosis in 5μM group was higher significantly than that in 1μM group (p 〈 0.01). The percentages of apoptosis in 5μM group was higher distinct than that in control group in A549 cell, but there was no difference between the 1μM group and control group in A549 cell. Condusion 9-cis-RA had distinct effects on growth inhibition differentiation and apoptosis induction in PG human lung glandular cancer cells and had weak effects on A549 cell.
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