Yildirim Erkan, Ozisik Kanat, Ozisik Pinar, Emir Mustafa, Yildirim Engin, Misirlioglu Müge, Tuncer Serdar, Kilinc Kamer
Thoracic Division, Ankara Numune Teaching and Research Hospital, Ankara, Turkey.
Heart Lung Circ. 2006 Apr;15(2):124-9. doi: 10.1016/j.hlc.2005.10.001. Epub 2006 Feb 21.
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.
Fifty-six Wistar-Albino female rats weighing 180-220 g 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.
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).
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.
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