Effect of Soyasaponin on Expression of Fas/FasL of Pneumonocyte in Silicotic Fibrosis Rats

  • Houjun Xu
  • Yulan Hao
  • Yu Su
  • Qingzhao Li
  • Jianhui Wu
  • Hongmin Fan
  • Manman Wang
  • Licheng Yan
  • Haijuan An
  • Yanshu Zhang
Conference paper
Part of the Lecture Notes in Electrical Engineering book series (LNEE, volume 204)

Abstract

Objectives to discuss the effect of SS on expression of Fas and FasL of Pneumonocyte in the Silicotic Fibrosis Rats. Methods Superoxide dismutase (SOD) and malondialdehyde (MDA) of pulmonary tissue and changes of that after SS intervened were observed. The immunohistochemical method was used to detect the level in the expressions of Fas and FasL protein. Results Compared with NS group, the level of SOD decreased constantly in SiO2 group (P < 0.05). MDA was increased significantly and maintain the high level (P < 0.05). Expression of Fas protein of SiO2 group was 4.51 and 5.05 times compared with its NS group. Its positive staining was located in epithelial cells of bronchi-duct and alveolar endothelial cells. Conclusions Fas and FasL system might take part in the pulmonary fibrosis. A certain dose of SS might down regulate the expressions of Fas and FasL to relieve the development of pulmonary fibrosis.

Keywords

Silicosis Pulmonary fibrosis Soyasaponin Fas FasL 

Notes

Acknowledgments

Hebei Province Key Labo- ratory of Occupational Health and safety for Coal Industry, Hebei United Univeristy, Tangshan Hebei Province, China, 063000. Science and technology research and development program of Tangshan City. (Grant No.10150 204A-36).

References

  1. 1.
    Borges VM, Lopes MF, Falcao H et al (2002) Apoptosis underlies immnopathogenic mechanisms in acute silicosis. Am J Physiol Lung Cell Mol Physiol 27:78–84Google Scholar
  2. 2.
    Yinping W, Jiayang W, Fenglan Z et al (1993) The influence to SOD and LPO of diabetic rat caused by soyasaponin andginsenosides from stems and leaves saponins. J Norman Bethune Univ Med Sci 19(2):122–123Google Scholar
  3. 3.
    Buccellato LJ, Tsa M, Akinci OI et al (2004) Reactive oxygen species are required hyperoxia-induced bax activation and cell death in alveolar epithelial cells. J Biochem 278(8):6753–6760Google Scholar
  4. 4.
    Distelhorst CW, Shore GC (2004) Bcl-2 and calcium: controversy beneath the surface. Oncog 23(16):2875–2880CrossRefGoogle Scholar
  5. 5.
    Li M, Cai JF, Chiu JF (2002) Arsenic induces oxidative stress and activates stress gene expressions in cultured lung epithelial cells. J Cell Biochem 87(1):29–38CrossRefGoogle Scholar
  6. 6.
    Sun JSH, Lu FJ, Huang WCH et al (1999) Antioxidant status following acute ischemia limb injury: a rabbit model. Free Radic Res 31(1):9–12CrossRefGoogle Scholar
  7. 7.
    Wanjun L, Shengxi C, Jiaxin H et al (1999) The influence of lipid peroxidation caused by reperfusion lung injury on ischemic preconditioning. Chin J Pathophysiol 15(8):27–29Google Scholar
  8. 8.
    Rieux-Laucat F, Le Deist F, Hovroz C et al (1995) Mutations in fas associated with human lymphoprolife active syndrome and autoimmunity. Sci 268:1347–1349CrossRefGoogle Scholar

Copyright information

© Springer-Verlag London 2013

Authors and Affiliations

  • Houjun Xu
    • 1
  • Yulan Hao
    • 1
  • Yu Su
    • 1
  • Qingzhao Li
    • 1
  • Jianhui Wu
    • 1
  • Hongmin Fan
    • 1
  • Manman Wang
    • 1
  • Licheng Yan
    • 1
  • Haijuan An
    • 1
  • Yanshu Zhang
    • 1
  1. 1.Hebei United UniveristyTangshan Hebei ProvinceChina

Personalised recommendations