Background and Purpose- Our recent study demonstrated that release of Prx2 (
peroxiredoxin 2) from red blood cells (RBCs) is involved in the inflammatory response and
brain injury after
intracerebral hemorrhage. The current study investigated the role of extracellular Prx2 in
hydrocephalus development after experimental intraventricular
hemorrhage. Methods- There were 4 parts in this study. First, Sprague-Dawley rats received an
intraventricular injection of lysed RBC or saline and were euthanized at 1 hour for Prx2 measurements. Second, rats received an
intraventricular injection of Prx2, deactivated Prx2, or saline. Third, lysed RBC was coinjected with
conoidin A, a Prx2 inhibitor, or vehicle. Fourth, rats received Prx2 injection and were treated with
minocycline or saline (i.p.). The effects of Prx2 and the inhibitors were examined using magnetic resonance imaging assessing ventriculomegaly, histology assessing ventricular wall damage, and immunohistochemistry to assess
inflammation, particularly at the choroid plexus. Results-
Intraventricular injection of lysed RBC resulted in increased brain Prx2 and
hydrocephalus.
Intraventricular injection of Prx2 alone caused
hydrocephalus, ventricular wall damage, activation of choroid plexus epiplexus cells (macrophages), and an accumulation of neutrophils.
Conoidin A attenuated lysed RBC-induced injury. Systemic
minocycline treatment reduced the epiplexus cell activation and
hydrocephalus induced by Prx2. Conclusions- Prx2 contributed to the intraventricular
hemorrhage-induced
hydrocephalus, probably by inducing inflammatory responses in choroid plexus and ventricular wall damage.