Effects of Juglone on ROS Production and Mitochondrial Transmembrane Potential in SGC-7901 Cells

Part of the Advances in Intelligent and Soft Computing book series (AINSC, volume 134)


To investigate the effects of juglone on ROS production and mitochondrial transmembrane potential (ΔΨm) in SGC-7901 cells in vitro, further to elucidate the apoptosis mechanism. The apoptosis morphological changes of SGC-7901 cells were observed using fluorescence microscope. The level of ROS and ΔΨm of cells were detected by FCM. The change of [Ca2 + ]i in cells stained with Fluo-3/AM was observed by LCSM. Hoechst 33258 staining assay showed thick granulated fluorescence in condensed nuclei and cytoplasm, and the number of apoptotic bodies was increased with increasing of juglone concentration. The level of ROS at the dose of 5, 10, 15 and 20μM of juglone was 34.83±1.45%, 42.43±1.36%, 53.73±1.38% and 68.67±1.33%, respectively, which were significantly higher than that in control group (P <0.01). The concentration of Ca2 + in cells exposed to juglone for 24 h was increased significantly in a dose dependent manner compared with control group (P <0.01). ΔΨm of treatment groups was 85.53±1.82%, 53.57±2.48%, 46.33±1.46%, 36.43±2.64%, respectively, which were significantly lower than that in control group (P <0.01).Therefore, juglone can increase intracellular level of ROS and concentration of Ca2 + , decrease ΔΨm and induce the cells apoptosis.


Juglone ROS Mitochondrial transmembrane potential Human gastric carcinoma SGC-7901 


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  1. 1.
    Sugie, S., Okamoto, K., Rahman, K.M., et al.: Inhibitory effects of plumbagin and juglone on azoxymethane-induced intestinal carcinogenesis in rats. Cancer Letters 127, 177–183 (1998)CrossRefGoogle Scholar
  2. 2.
    Kamei, H., Koide, T., Kojima, T., et al.: Inhibition of cell growth in culture by quinones. Cancer Biotherapy and Radiopharmaceuticals 13, 185–188 (1998)CrossRefGoogle Scholar
  3. 3.
    Segura-Aguilar, J., Jonsson, K., Tidefelt, U., et al.: The cytotoxic effects of 5-OH-1,4-naphthoquinone and 5,8-diOH-1,4-naphthoquinone on doxorubicin-resistant human leukemia cells (HL-60). Leukemia Research 16, 631–637 (1992)CrossRefGoogle Scholar
  4. 4.
    Bolton, J.L., Trush, M.A., Penning, T.M., et al.: Role of quinones in toxicology. Chemical Research in Toxicology 13, 135–160 (2000)CrossRefGoogle Scholar
  5. 5.
    Bhuyan, K.C., Bhuyan, D.K., Podos, S.M.: Free radical enhancer xenobiotic is an inducer of cataract in rabbit. Free Radical Research Communications 12-13, 609–620 (1991)CrossRefGoogle Scholar
  6. 6.
    Monks, T.J., Hanzli, R.P.K., Cohen, G.M., et al.: Quinone chemistry and toxicity. Toxicol. Appl. Fharmacol. 112, 2–16 (1992)CrossRefGoogle Scholar
  7. 7.
    Babich, H., Stern, A.: In vitro cytotoxicities of 1,4-naphthoquinone and hydroxylated 1,4-naphthoquinones to replicating cells. Journal of Applied Toxicology 13, 353–358 (1993)CrossRefGoogle Scholar
  8. 8.
    Ito, K., Nakazato, T., Yamato, K., et al.: Induction of apoptosis in leukemic cells by homovanillic acid derivative capsaicin through oxidative stress implication of phosphorylation of p53 at Ser-15 residue by reactive oxygen species. Cancer Research 64, 1071–1078 (2004)CrossRefGoogle Scholar
  9. 9.
    Das, R., Roy, A., Dutta, N., et al.: Reactive oxygen species and imbalance of calcium homeostasis contributes to curcumin induced programmed cell death in Leishmania donovani. Apoptosis 13, 867–882 (2008)CrossRefGoogle Scholar
  10. 10.
    Kroemer, G., Dallaporta, B., Resche Rigon, M.: The mitochondrial death/life regulator in apoptosis and necrosis. Annual Review of Physiology 60, 619–642 (1998)CrossRefGoogle Scholar
  11. 11.
    Li, P., Nijhawan, D., Budihardjo, I., et al.: Cytochrome c and dATP-dependent formation of Apaf-1/caspase-9 complex initiates an apoptotic protease cascade. Cell 91, 479–489 (1997)CrossRefGoogle Scholar
  12. 12.
    Launay, S., Hermine, O., Fontenay, M., et al.: Vital functions for lethal caspases. Oncogene 24, 5137–5148 (2005)CrossRefGoogle Scholar

Copyright information

© Springer-Verlag GmbH Berlin Heidelberg 2012

Authors and Affiliations

  • Yubin Ji
    • 1
  • Zhongyuan Qu
    • 1
  • Xiang Zou
    • 2
  • Chenfeng Ji
    • 2
  1. 1.Institute of Materia Medica and Postdoctoral ProgrammeHarbin University of CommerceHarbinChina
  2. 2.Engineering Reseach Center of Natural Anticancer DrugsMinistry of EducationHarbinChina

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