陈辉星, 陈燕凌. 幽门螺杆菌通过Bcl-2/Bax机制诱导HepG2细胞凋亡的研究[J]. 中国肿瘤临床, 2012, 39(19): 1393-1396. DOI: 10.3969/j.issn.1000-8179.2012.19.001
引用本文: 陈辉星, 陈燕凌. 幽门螺杆菌通过Bcl-2/Bax机制诱导HepG2细胞凋亡的研究[J]. 中国肿瘤临床, 2012, 39(19): 1393-1396. DOI: 10.3969/j.issn.1000-8179.2012.19.001
Huixing CHEN, Yanling CHEN. Bcl-2/Bax Induced Apoptosis of HepG2 Cells by Helicobacter pylori[J]. CHINESE JOURNAL OF CLINICAL ONCOLOGY, 2012, 39(19): 1393-1396. DOI: 10.3969/j.issn.1000-8179.2012.19.001
Citation: Huixing CHEN, Yanling CHEN. Bcl-2/Bax Induced Apoptosis of HepG2 Cells by Helicobacter pylori[J]. CHINESE JOURNAL OF CLINICAL ONCOLOGY, 2012, 39(19): 1393-1396. DOI: 10.3969/j.issn.1000-8179.2012.19.001

幽门螺杆菌通过Bcl-2/Bax机制诱导HepG2细胞凋亡的研究

Bcl-2/Bax Induced Apoptosis of HepG2 Cells by Helicobacter pylori

  • 摘要:
      目的  探讨幽门螺杆菌(H.pylori)对肝细胞HepG2细胞凋亡的影响及其机制。
      方法  应用HepG2细胞为实验模型, 用MTT、荧光染色技术、透射电子显微镜、AO/EB染色、流式细胞仪定性和定量地检测HepG2细胞凋亡情况; Western Blotting法检测凋亡相关蛋白Bcl-2和Bax蛋白的表达。
      结果  不同浓度H.pylori处理组(4.0×105、4.0×106、4.0×107和4.0×108CFU/mL)的24 h细胞生长抑制率分别为(2.64±0.34)%、(16.35+4.24)%、(27.15±3.19)%和(33.35±2.36)%(P < 0.05), 抑制率随作用时间的延长而增加(P < 0.05)。HepG2细胞与4×107/mL浓度的NCTC11637共培养24h后, 在透射电镜下可见部分细胞呈不同时期的凋亡形态。不同浓度H.pylori的凋亡率分别为(2.50±0.45)%、(6.00±0.35)%、(11.10±0.45)%和(14.65±0.27)%, 当H.pylori的浓度≥4.0×106CFU/mL, HepG2细胞凋亡率与对照组比较差异有统计学意义(P < 0.05)。H.pylori作用HepG2细胞后, HepG2细胞的Bcl-2蛋白表达明显减少, Bax蛋白表达则与Bcl-2蛋白表达情况相反。
      结论  H.pylori通过Bcl-2/Bax机制诱导HepG2细胞凋亡。

     

    Abstract:
      Objective  This study investigated the effects of live Helicobacter pylori on the apoptosis of the human hepatoma cells (HepG2).
      Methods  The effect of the co-incubation with different concentrations of the H.pylori NCTC11637 strain(4.0×105, 4.0×106, 4.0×107 and 4.0×108 CFU/ml) for 24 h on the apoptotic rates of HepG2 cells were investigated by the MTT assay, fluorescence imaging, ultrastructural analysis, and flow cytometry.
      Results  H.pylori significantly inhibited the HepG2 cell growth in a dose-dependent manner (P < 0.05).The respective inhibition ratios were(2.64±0.34)%, (16.35±4.24)%, (27.15±3.19)%, and(33.35±2.36)%, in the order of increasing NCTC11637 concentrations, after 24 h of incubation.H.pylori promoted the apoptosis of HepG2 cells, and this effect was enhanced with the increased bacterial concentration.The different phases of the apoptosis were observed after the co-incubation with H.pylori using an electron microscope.The respective apoptotic rates of the HepG2 cells were(2.50±0.45)%, (6.00±0.35)%, (11.10±0.45)%, and(14.65±0.27)%after 24 h of incubation with the increasing NCTC11637 concentrations.Differences in the apoptotic rates that were higher than(2.50±0.45)%were considered significant(P < 0.05).The Bcl-2 protein levels were inhibited, whereas the Bax protein levels were increased in the HepG2 cells after treatment with H.pylori.
      Conclusion  The co-incubation of HepG2 cells with H.pylori increases their rate of apoptosis in a concentration-dependent manner through the Bcl-2/Bax mechanism.

     

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