Background: Oxidative stress has been implicated in the pathophysiology of cerebral ischemia.
Pentraxin-3 plays an important role in innate immune responses and in inflammatory
diseases. Our aim was to evaluate pentraxin-3 serum level on focal transient cerebral
ischemia and reperfusion model in rabbits and to assess the anti-inflammatory and
anti-oxidant effects of vagus nerve stimulation. Materials and methods: Focal transient cerebral ischemia and reperfusion was induced by occlusion of the
right common carotid artery for 2 hours followed by reperfusion for one hour. Stimulating
electrodes were implanted on the cervical part of the right vagus nerve. Vagus nerve
stimulation was started 30 min following right common carotid artery ligation for
a period of one hour. The stimulation signals were delivered every five minutes for
30 seconds. All the procedures were duplicated but no stimulus was delivered in the
control group. Serum level of pentraxin-3, lipid peroxide and total thiols were determined
at baseline, at end of ischemia and at end of reperfusion and the animal decapitated
and neuronal damage was evaluated. Results: We found that vagus nerve stimulation caused reduction of the ischemic features with
revival of the cell shape and size. It also resulted in decreased serum levels of
pentraxin-3 and lipid peroxide whereas the level of total thiols was increased. Conclusion: We concluded that the observed diversity in pentraxin-3, lipid peroxide and total
thiols serum levels in cerebral ischemia and reperfusion may reflect relative roles
in the biology. Anti-inflammatory and anti-oxidant role of vagus nerve stimulation
in cerebral ischemia and reperfusion may represent a marker of altered cerebral function,
and may provide potential therapeutic applications.
Key-words:
Cerebral ischemia and Reperfusion - pentrax-in-3 - Vagus nerve stimulation.
