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苦参碱诱导HL-60细胞株凋亡作用的实验研究 被引量:4

Apoptosis of cell line HL-60 induced by matrine
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摘要 目的研究苦参碱(MAT)诱导HL-60细胞株凋亡的作用及其机制。方法采用CCK-8法检测不同浓度MAT对HL-60细胞的增殖抑制作用;流式细胞术检测细胞凋亡以及线粒体跨膜电位的变化;分光光度法检测Caspase-9活性。结果0.25~2.0mg/mlMAT对HL.60细胞有生长抑制作用,与对照组相比差异有统计学意义(F=67.83,P〈0.05);MAT处理48h后,细胞凋亡率明显增高,并呈剂量依赖性(t值分别为4.685、6.300、9.641、6.786,均P〈0.05);1.0mg/mlMAT处理后48h内,细胞线粒体跨膜电位逐渐降低(F=54.83,P〈0.05),Caspase-9活性逐渐升高,呈时间依赖性(F=72.31,P〈0.05)。结论MAT可能通过降低细胞线粒体跨膜电位、激活Caspase-9而诱导HL-60细胞凋亡。 Objective To investigate the apoptosis of cell line HL-60 induced by matrine and its possible mechanism. Methods CCK-8 assay was used to observe the proliferation inhibitation of HL-60 cells treated with matrine. FCM was applied to detect apoptotic cells and mitochondrial transmembrane potential. Spectrophotometry was used to detect the activity of Caspase-9. Results Matrine (0.25-2.0 mg/ml) could significantly inhibit proliferation of HL-60 cells (F=67.83, P 〈0.05). After 48 hours, the apoptosis rate increased obviously in dose dependence (t = 4.685, 6.300. 9.641, 6.786, P 〈0.05). Within 48 hours, the mitoehondrial transmembrance potential of HL-60 cells treated with matrine (1.0 mg/ml) gradually decreased (F = 54.83, P 〈0.05), and the activation of Caspase-9 gradually decreased in time dependence (F = 72.31, P 〈0.05). Conclusion Matrine can induce apoptosis of HL-60 cells by reducing mitochondrial transmembrance potential and activating Caspase-9.
出处 《白血病.淋巴瘤》 CAS 2011年第8期480-481,489,共3页 Journal of Leukemia & Lymphoma
关键词 苦参碱 HL-60细胞 细胞凋亡 Matrine HL-60 cells Apoptosis
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  • 1李向阳,僧靖静,赵高峰,僧国珍.胃腺癌TSP-1的表达与细胞胀亡的关系及意义[J].中国现代普通外科进展,2005,8(1):34-36. 被引量:3
  • 2刘伟,僧靖静,赵高峰,王公平,杨振,僧国珍,高冬玲,张云汉.胃肠道恶性肿瘤中细胞胀亡的检测及意义[J].临床外科杂志,2006,14(5):299-300. 被引量:2
  • 3牛万成,李玺.外源性ATP对大鼠移植胰腺的作用及机制[J].第四军医大学学报,2006,27(16):1477-1479. 被引量:2
  • 4Fritz Dünschede,Kirsten Erbes,Achim Kircher,Stefanie Westermann,Joachim Seifert,Arno Schad,Kempski Oliver,Alexandra K Kiemer,Junginger Theodor.Reduction of ischemia reperfusion injury after liver resection and hepatic inflow occlusion by α-lipoic acid in humans[J].World Journal of Gastroenterology,2006,12(42):6812-6817. 被引量:6
  • 5Morin D,Pires F,Plin C,et al.Role of the permeability transition pore in cytochrome C release from mitochondria during ischemia-reperfusion in rat liver[J].Biochem Pharmacol,2004,68(10):2065-2073.
  • 6Kumarswamy R,Chandna S.Putative partners in Bax mediated cytochrome-Crelease:ANT,CypD,VDAC or none of them[J] ?Mitochondrion,2009,9(1):1-8.
  • 7Banerjee J,Ghosh S.Bax increases the pore size of rat brain mitochondrial voltage-dependent anion channel in the presence of tBid[J].Biochem Biophys Res Commun,2004,323(1):310-314.
  • 8Shimizu S,Matsuoka Y,Shinohara Y,et al.Essential role of voltage-dependent anion channel in various forms of apoptosis in mammalian cells[J].J Cell Biol,2001,152(2):237-250.
  • 9Pastorino JG,Shulga N,Hoek JB.Mitochondrial binding of hexokinase II inhibits Bax-induced cytochrome-C release and apoptosis[J].J Biol Chem,2002,277(9):7610-7618.
  • 10Shimizu S,Shinohara Y,Tsujimoto Y.Bax and Bcl-xL independently regulate apoptotic changes of yeast mitochondria that require VDAC but not adenine nucleotide translocator[J].Oncogene,2000,19(38):4309-4318.

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