Heart, Lung and Circulation
Volume 15, Issue 2 , Pages 124-129, April 2006

Apoptosis-Related Gene Bcl-2 in Lung Tissue After Experimental Traumatic Brain Injury in Rats

  • Erkan Yildirim, MD, FETCS

      Affiliations

    • Thoracic Division, Ankara Numune Teaching and Research Hospital, Ankara, Turkey
    • Corresponding Author InformationCorresponding author. Tel.: +90 312 310 30 30/3004–3005; fax: +90 312 484 62 04; mobile: +90 532 445 39 38.
    • ,
  • Kanat Ozisik, MD

      Affiliations

    • Department of Cardiovascular Surgery, Ankara Numune Teaching and Research Hospital, Ankara, Turkey
    • ,
  • Pinar Ozisik, MD

      Affiliations

    • Hacettepe University, Institute of Neurological Sciences and Psychiatry, Ankara, Turkey
    • ,
  • Mustafa Emir, MD

      Affiliations

    • Department of Cardiovascular Surgery, TYIH, Ankara, Turkey
    • ,
  • Engin Yildirim, MD

      Affiliations

    • Department of Pharmacology, School of Medicine, Osmangazi University, Eskişehir, Turkey
    • ,
  • Müge Misirlioglu, PhD

      Affiliations

    • Metis Biotechnology, Ltd., Ankara, Turkey
    • ,
  • Serdar Tuncer, MD

      Affiliations

    • Metis Biotechnology, Ltd., Ankara, Turkey
    • ,
  • Kamer Kilinc, MD

      Affiliations

    • Department of Biochemistry, Faculty of Medicine, Hacettepe University, Ankara, Turkey

Received 22 May 2005; received in revised form 2 October 2005; accepted 3 October 2005.

Background

We have recently shown that experimental traumatic brain injury resulted in ultra structural damage in lung tissue. The main objective of the current study was to investigate in a rat model of brain injury whether expression of Bcl-2 gene and lipid peroxidation levels in the lung tissue after traumatic brain injury were affected by methylprednisolone sodium succinate (MPSS) treatment.

Methods

Fifty-six Wistar-Albino female rats weighing 180–220g were used, which were allocated into seven groups. A weight-drop method was used to achieve head trauma. Real time quantitative PCR analyses for Bcl-2 gene expression and measurement of the levels of lipid peroxidation were carried out. All the data was analyzed by using SPSS 11.5 for Windows.

Results

Mean Bcl-2 expression in the methylprednisolone group was considerably higher compared to that of all the other groups (p<.05). Mean lipid peroxidation levels were significantly higher in the trauma group and notably lower in the methylprednisolone group (p<.01).

Conclusions

The oxidative stress imposed on lung tissue, as seen by high levels of lipid peroxidation, after brain injury was significantly attenuated by MPSS treatment. MPSS treatment following brain injury also augmented putative anti-apoptotic Bcl-2 gene expression in lung tissue. Further studies are required to determine the full range and lower limits of effective MPSS dose. More importantly the optimal efficacy according to the timing of MPSS treatment after brain injury needs to be determined for impact on more diverse markers of cell inflammation, apoptosis and injury.

Keywords: Trauma, Blunt, Animal model, Brain, Lung, Apoptosis, Lung transplantation

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PII: S1443-9506(05)00207-6

doi:10.1016/j.hlc.2005.10.001

Heart, Lung and Circulation
Volume 15, Issue 2 , Pages 124-129, April 2006

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