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Hyperbaric oxygenation alters temporal expression pattern of superoxide dismutase 2 after cortical stab injury in rats
Ana B. Parabucki
; Department of Neurobiology Institute for Biological Research “Siniša Stanković,” University of Belgrade, Serbia
Iva D. Božić
; Department of Neurobiology Institute for Biological Research “Siniša Stanković,” University of Belgrade, Serbia
Ivana M. Bjelobaba
; Department of Neurobiology Institute for Biological Research “Siniša Stanković,” University of Belgrade, Serbia
Irena C. Lavrnja
; Department of Neurobiology Institute for Biological Research “Siniša Stanković,” University of Belgrade, Serbia
Predrag D. Brkić
; Institute of Medical Physiology “Richard Burian,” School of Medicine, University of Belgrade, Belgrade, Serbia
Tomislav S. Jovanović
; Institute of Medical Physiology “Richard Burian,” School of Medicine, University of Belgrade, Belgrade, Serbia
Danijela Z. Savić
; Department of Neurobiology Institute for Biological Research “Siniša Stanković,” University of Belgrade, Serbia
Mirjana B. Stojiljković
; Department of Neurobiology Institute for Biological Research “Siniša Stanković,” University of Belgrade, Serbia
Sanja M. Peković
; Department of Neurobiology Institute for Biological Research “Siniša Stanković,” University of Belgrade, Serbia
Sažetak
Aim To evaluate the effect of hyperbaric oxygen therapy
(HBOT) on superoxide dismutase 2 (SOD2) expression pattern
after the cortical stab injury (CSI).
Methods CSI was performed on 88 male Wistar rats, divided
into control, sham, lesioned, and HBO groups. HBOT
protocol was the following: pressure applied was 2.5 absolute
atmospheres, for 60 minutes, once a day for consecutive
3 or 10 days. The pattern of SOD2 expression and cellular
localization was analyzed using real-time polymerase
chain reaction, Western blot, and double-label fluorescence
immunohistochemistry. Neurons undergoing degeneration
were visualized with Fluoro-Jade®B.
Results CSI induced significant transient increase in SOD2
protein levels at day 3 post injury, which was followed by
a reduction toward control levels at post-injury day 10. At
the same time points, mRNA levels for SOD2 in the injured
cortex were down-regulated. Exposure to HBO for 3 days
considerably down-regulated SOD2 protein levels in the
injured cortex, while after 10 days of HBOT an up-regulation
of SOD2 was observed. HBOT significantly increased
mRNA levels for SOD2 at both time points compared to
the corresponding L group, but they were still lower than
in controls. Double immunofluorescence staining revealed
that 3 days after CSI, up-regulation of SOD2 was mostly
due to an increased expression in reactive astrocytes surrounding
the lesion site. HBOT attenuated SOD2 expression
both in neuronal and astroglial cells. Fluoro-Jade®B
labeling showed that HBOT significantly decreased the
number of degenerating neurons in the injured cortex.
Conclusion HBOT alters SOD2 protein and mRNA levels
after brain injury in a time-dependent manner.
Ključne riječi
Hrčak ID:
95436
URI
Datum izdavanja:
15.12.2012.
Posjeta: 983 *