Effect of Recombinant Human Lipocortin I on Brain Oedema in a Rat Glioma Model

  • C. C. Chang
  • M. Shinonaga
  • T. Kuwabara
  • T. Mima
  • T. Shigeno
Conference paper
Part of the Acta Neurochirurgica book series (NEUROCHIRURGICA, volume 51)


Glucocorticoids have been extensively used to treat brain oedema, but little is known on the mechanisms of steroids in the prevention and resolution of tumour-induced brain oedema. Recently, the mechanism of steroid action is thought to involve synthesis of proteins with antiphospholipase activity called lipocortins. In a previous study, we have demonstrated the efficacy of dexamethasone (DEX) in resolving peritumoural oedema in a rat glioma model. Using the same model, we studied the effect of recombinant human lipocortin I on the resolution of peritumoural oedema.

Intracerebral tumours were produced in 6-week-old Wistar rats by implantation of rat glioma C6 cells. In comparison with sham-operated controls, the tumour-implanted animals showed significant increase in the cortical water content, which was reduced by DEX administration to the level in the sham-operated controls. The water content within the tumour was also significantly decreased by DEX treatment. On the other hand, there was no difference in water content between lipocortin-treated and non-treated animals. These findings suggest that tumour-induced brain oedema can be reduced by DEX treatment but not by lipocortin.

In conclusion, it is doubtful whether glucocorticoids exert their action in resolving brain oedema by inducing PLA2 inhibitory proteins named lipocortins.


Brain Oedema Intracerebral Tumour Human Umbilical Artery Peritumoural Oedema Nontreated Animal 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.


Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.


  1. 1.
    Chang CC (1989) Neurotransmitter amines in brain oedema of a rat glioma model. Neurol Med Chir (Tokyo) 29: 187–191CrossRefGoogle Scholar
  2. 2.
    Cirino G, Flower RJ (1987) Human recombinant lipocortin I inhibits prostacyclin production by human umbilical artery in vitro. Prostaglandins 34: 59–62PubMedCrossRefGoogle Scholar
  3. 3.
    Cirino G, Flower RJ, Browing JL, Sinclair LK, Pepinsky RB (1987) Recombinant human lipocortin I inhibits thromboxane release from guinea-pig isolated perfused lung. Nature (Lond) 328: 270–272CrossRefGoogle Scholar
  4. 4.
    DiRosa M, Flower RJ, Hirata F, Parente L, Russo-Marie F (1984) Nomenclature announcement. Anti-phospholipase proteins. Prostaglandins 28: 441–442CrossRefGoogle Scholar
  5. 5.
    Fishman RA (1975) Brain oedema. N Engl J Med 293: 706–711PubMedCrossRefGoogle Scholar
  6. 6.
    Fishman RA (1982) Steroids in the treatment of brain oedema. N Engl J Med 306: 359–360PubMedCrossRefGoogle Scholar
  7. 7.
    Flower RJ (1984) Macrocortin and the antiphospholipase proteins. Adv Inflamm Res 8: 1–34Google Scholar
  8. 8.
    Hossmann A, Wechsler W, Wilmes F (1979) Experimental peritumourous oedema. Acta Neuropathol (Berl) 45: 195–203CrossRefGoogle Scholar
  9. 9.
    Klatzo I (1967) Neuropathological aspects of brain oedema. J Neuropath Exp Neurol 26: 1–14PubMedCrossRefGoogle Scholar
  10. 10.
    Northup JK, Valentine-Braun KA, Johnson LK, Severson DL, Hollenberg MD (1988) Evaluation of the antiinflammatory and phospholipase-inhibitory activity of calpactin II/lipocortin I. J Clin Invest 82: 1347–1352PubMedCrossRefGoogle Scholar

Copyright information

© Springer-Verlag 1990

Authors and Affiliations

  • C. C. Chang
    • 1
  • M. Shinonaga
    • 2
  • T. Kuwabara
    • 2
  • T. Mima
    • 2
  • T. Shigeno
    • 3
  1. 1.Department of NeurosurgeryYokohama City University School of MedicineMinami-ku, Yokohama 232Japan
  2. 2.University TokyoJapan
  3. 3.Saitama Medical CenterJapan

Personalised recommendations