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芬太尼和瑞芬太尼对人肺癌A549细胞活力的影响 被引量:9

Effects of fentanyl and remifentanil on viability of human adenocarcinoma cell line A549
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摘要 目的评价芬太尼和瑞芬太尼对人肺癌A549细胞活力的影响。方法人肺癌A549细胞培养至对数生长期,接种于96孔培养板或75ml培养瓶中,采用随机数字表法,将其随机分为9组(n=30):不同浓度芬太尼组(F1-4组)芬太尼终浓度分别为0.5、5.0、50.0、500.0ng/ml,不同浓度瑞芬太尼组(RF1-4组)瑞芬太尼终浓度分别为0.5、50、50.0、500.0ng/ml,正常对照组(c组j加入等容量的RPMll640培养基。分别于孵育24、48和72h时,采用噻唑蓝比色法测定细胞活力;于孵育24h时经AnnexinV—FITC/PI双标记染色后,采用流式细胞仪检测细胞凋亡率,经PI染色后,采用流式细胞仪检测细胞周期分布。结果C组、F2-4组或RF2-4组孵育72h时人肺癌A549细胞活力依次降低,孵育24h时s期比例依次降低,G2/M期比例和凋亡率依次升高(P〈0.05)。结论芬太尼和瑞芬太尼终浓度≥5ng/ml时,可浓度依赖性地抑制人肺癌A549细胞活力,其机制可能与诱导细胞凋亡,使细胞周期停滞于G2/M期有关。 Objective To investigate the effects of fentanyl and remifentanil on the viability of human adenocarcinoma cell line A549. Methods Human adenocarcinoma A549 ceils cultured in logarithmic growth phase were seeded in 75 ml culture bottles or 96-well plates. After being cultured for 24 h, the cells were randomly divided into 9 groups (n = 30 each): 4 fentanyl groups (groups F2-4 ), 4 remifentanil groups (groups RF2-4 ) and control group (group C). Groups F1-4 were exposed to fentanyl with the final concentrations of 0.5, 5.0, 50.0 and 500.0 ng/ml respectively. Groups RF1-4 were exposed to remifentanil with the final concentrations of 0.5, 5.0, 50.0 and 500.0 ng/ml respectively. The viability of the ceils was determined by methyl thiazolyl tetrazolium assay after being incubated for 24, 48 and 72 h. The cell cycle progression and apoptosis were determined by flow cytometry after being incubated for 24 h. Results Compared with group C, the viability of A549 cells were gradually decreased at 72 h of incubation, the proportion of the cells in S phase was gradually decreased at 24 h of incubation, and the proportion of the cells in G2/M phase and apoptotic rate were gradually increased in groups F2-4 and in groups RF2-4 ( P 〈 0.05). Conclusion Fentanyl and remifentanil with the final concentration ≥ 5 ng/ml can inhibit the viability of human adenoearcinoma cell line A549 in a dose-independent manner by inducing cell apoptosis and cell cycle arrest in G2/M phase.
出处 《中华麻醉学杂志》 CAS CSCD 北大核心 2012年第7期817-819,共3页 Chinese Journal of Anesthesiology
基金 河北省高等学校强势特色学科(2005-52) 河北省卫生厅重点学科跟踪项目(GL200737) 河北省自然科学基金(c2008000967)
关键词 芬太尼 哌啶类 细胞系 肿瘤 细胞存活 Fentanyl Piperidines Cell line, tumor Cell survival
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参考文献8

  • 1Ishikawa M, Tanno K, Kamo A, et al. Enhancement of tumor growth by morphine and its possible mechanism in mice. Biol Ptmrm Bull, 1993, 16(8) :762-766. 被引量:1
  • 2Sueoka E, Sueoka N, Kai Y, et al. Anticancer activity of morphine and its synthetic derivative, KT-90, mediated through apoptosis and inhibi- tion of NF-kappa B activation. Bioehem Biophys Res Commun, 1998, 252(3) :566-570. 被引量:1
  • 3Stefano GB, Kream RM, Mantione KJ, et al. Endogenous morphine ni- tric oxide-coupled regulation of cellular physiology and gene expres- sion: implications for cancer biology. Semin Cancer Biol, 2008, 18 (3) : 199-210. 被引量:1
  • 4Hatsukari I, Hitosugi N, Matsumoto I, et al. Induction of early apopto- sis marker by morphine in human lung and breast carcinoma cell lines. Anticancer Res, 2003,23 ( 3 B) : 2413-2417. 被引量:1
  • 5Tegeder I, Grosch S, Schmidtko A, et al. G protein-independence GI cell cycle block and apoptosis with morphine in adenocarcinoma cell: involvement of 53 phosphorylation. Cancer Res, 2003,63 ( 8 ) : 1846- 1852. 被引量:1
  • 6Zagon IS, Molaughlin PJ. Opioids and the apoptotic pathway in human cancer cells. Neuropeptides, 2003,37 (2) : 79-88. 被引量:1
  • 7Hitosugi N, Nagasaka H, Sakagami H, et al. Analysis of apoptosis sig- naling pathway in human cancer cells by codeinone, a synthetic deriv- ative of codeine. Anticancer Res,2003(3B):2569-2576. 被引量:1
  • 8丁汉琳,张咸伟,张传汉.芬太尼影响MCF7细胞凋亡的实验研究[J].实用医学杂志,2004,20(12):1351-1353. 被引量:16

二级参考文献7

  • 1Sueoka E, Sueoka N, Kai Y, et al. Anticancer activity of morphine and its synthetic derivative, KT-90, mediated through apoptosis and inhibition of NF-kappa B activation. Biochem Biophys Res Commun, 1998, 252(3): 566-570 被引量:1
  • 2Boronat MA, Garcia-Fuster MJ, Garcia-Sevilla JA. Chronic morphine induces up-regulation of the pro-apoptotic Fas receptor and down-regulation of the anti-apoptotic Bcl-2 oncoprotein in rat brain. Br J Pharmacol, 2001, 134(6):1263-1270 被引量:1
  • 3Ishikawa M, Tanno K, Kamo A, et al. Enhancement of tumor growth by morphine and its possible mechanism in mice. Biol Pharm Bull, 1993, 16(8):762-766 被引量:1
  • 4Hatsukari I, Hitosugi N, Matsumoto I, et al. Induction of early apoptosis marker by morphine in human lung and breast carcinoma cell lines. Anticancer Res, 2003, 23(3B): 2413-2417 被引量:1
  • 5Zagon IS, McLaughlin PJ. Opioids and the apoptotic pathway in human cancer cells. Neuropeptides, 2003, 37(2): 79-88 被引量:1
  • 6Tegeder I, Grosch S, Schmidtko A, et al. G protein-independence G1 cell cycle block and apoptosis with morphine in adenocarcinoma cell: involvement of 53 phosphorylation. Cancer Res, 2003, 63(8): 1846-1852 被引量:1
  • 7Hitosugi N, Nagasaka H, Sakagami H, et al. Analysis of apoptosis signaling pathway in human cancer cells by codeinone, a synthetic derivative of codeine. Anticancer Res, 2003, 23(3B): 2569-2576 被引量:1

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