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机构地区:[1]三峡大学第一临床医学院 [2]宜昌市第三人民医院,湖北宜昌443003
出 处:《中国现代医学杂志》2008年第16期2327-2329,共3页China Journal of Modern Medicine
摘 要:目的探讨蛋白激酶C(protein kinasec,PKC)抑制剂staurosporine(STS)对人结肠癌细胞株COLO320的增殖抑制、凋亡诱导及对细胞周期的影响。方法在培养的COLO320细胞中,加20、60及100ng/mLSTS和100ng/mL佛波酯(PMA),作用24h后,用MTT法测细胞增殖,流式细胞仪检测细胞凋亡率及细胞周期的变化。结果STS抑制COLO320细胞生长,24h的IC50为55ng/mL。20、60及100ng/mLSTS分别作用细胞24h后,发现G0/G1期细胞分别为(47.30%±1.53%)、(49.50%±1.54%)和(51.60%±2.12%),G2/M期细胞分别为(30.45%±1.32%)、(34.50%±1.23%)和(37.70%±1.82%);100ng/mLPMA组G0/G1期细胞为(57.10%±1.89%),G2/M期细胞为(24.70%±0.35%);空白对照组G0/G1期细胞为(50.60%±1.69%),G2/M期细胞为(1.85%±0.78%)。20、60及100ng/mLSTS组与100ng/mLPMA组及空白对照组比较,STS使细胞G0/G1期均减少(P<0.05)及G2/M期均明显增加(P<0.01)。STS作用24h后细胞的G1期前出现明显的凋亡峰。结论STS通过抑制PKC的活性,使细胞被阻滞于G2期,从而抑制COLO320细胞的增殖及诱导细胞凋亡。[Objective] To investigate the effect of PKC inhibitor staurosporine (STS) on the inhibition of proliferation, the induction of apoptosis, and the change of cell cycle in human colon cancer line COLO 320. [Methods] COLO320 ceils were treated by PKC inhibitor Staurosporine(STS) for 24 hours, the inhibition rates of ceil proliferation were evaluated by MTT assay. The apoptotic peaks of the ceils and the changes of ceil cycle were analyzed using flow cytometry. [Results] Stanrospofine inhibited ceil growth of COLO320, IC50 of 24 hours was 55 ng/mL. COLO320 ceils were treated by STS at the concentrations of 20,60 100 ng/ml for 24 hours, the percentages of G0/G1 phage were(47.3%±1.53%), (49.5%±1.54%), (51.6%±2.12%), respectively(57.1%±1.89%) in 100 ng/mL PMA, (50.6%±1.69%) in control group, the percentages of G2/M phage were (30.45%±1.32%), (34.5%±1.23%), (37.7%± 1.82%), respectively(24.7%±0.35%) in 100 ng/mL PMA, (1.85%±0.78%) in control group. Compared with the control group and PMA treated group, the percentages of G0/G1 phage of COLO320 decreased (P 〈0.05) and that of G2/M cells increased significantly in the STS treated group (P 〈0.01). Treated by STS at the different concentrations, the apoptotic peaks and typical apoptotic bodies were observed. [Condusion] STS significantly inhibits the proliferation, induces apoptosis of COLO320 cell and induces G2/M phase arrest by inhibiting the activation of PKC.
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