The acute
inflammatory response plays an important role in secondary brain
damage after traumatic brain injury (TBI). Neutrophils provide the
main source of matrix metalloproteinases (MMPs) which also play a
deleterious role in TBI. Numerous preclinical studies have suggested
that hyperbaric oxygen therapy (HBOT) may by beneficial in various
noncerebral and cerebral inflammatory diseases.
The goal of this
study was to evaluate the effects of HBOT on inflammatory
infiltration and the expression of MMPs in correlation with
secondary cell death in the rat model of dynamic cortical
deformation (DCD).
Twenty animals underwent DCD with subsequent HBOT (2.8 ATA, two
sessions of 45 min each); 10 animals: DCD and normobaric oxygenation
(1 ATA), 10 animals: not treated after DCD. Cell death was evaluated
by TUNEL.
Neutrophils were
revealed by myeloperoxidase staining. Immunohistochemical staining
for MMP-2 and -9 and tissue inhibitors of MMP-1 (TIMP-1) and -2 was
also performed and the results were quantitatively evaluated by
image analysis. In the animals treated by HBOT, a significant
decrease in the number of TUNEL-positive cells and neutrophilic
inflammatory infiltration was seen in comparison with nontreated
animals and those treated by normobaric oxygen. The expression of
MMP-9 was also significantly lower in the treated group. Staining
for MMP-2 and TIMP-2 did not change significantly.
Our results
demonstrate that HBOT decreased the extent of secondary cell death
and reactive neuroinflammation in the TBI model. The decline of
MMP-9 expression after HBOT may also contribute to protection of
brain tissue in the perilesional area. Further research should be
centred on the evaluation of long-term functional and morphological
results of HBOT.
Chesapeake,
Virginia
Mandurah, Victoria
Bahamas, Nassau
Portsmouth, Virginia
Seattle, Washington
Bundaberg, Queensland
Torrance, California
Poland, Warsaw
Comoros, Moroni (on Grande Comoro)
Abu Dhabi, United Arab Emirates, Abu Dhabi, UAE
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