Abstract
To study the effect of endothelial progenitor cell (EPC) treatment on intracerebral hemorrhage (ICH) in rats and elucidate possible mechanisms. The rats were randomly divided into three groups: (1) EPC group: ICH + EPC, (2) phosphate-buffered saline group: ICH + PBS, and (3) sham group. EPCs were transplanted intravenously 6 h after ICH. Modified neurological severity score was used to evaluate neurological function. Blood-brain barrier (BBB) integrity was evaluated. Dead cells, inflammatory cytokines, and neuroprotective cytokines were assessed to investigate possible mechanisms. The animals in the EPC group showed significant improvement in neurological function at 48 h, 72 h, and 7 days after ICH, compared with those in the PBS group. EPC transplantation significantly reduced brain edema and the number of dead cells in the hematoma boundary areas. The intensity of Evans Blue was decreased, and expression levels of zonula occluden-1 and claudin-5 were increased in the EPC group. Proinflammatory cytokines, including interferon-γ, IL-6, and TNF-α, were decreased, whereas anti-inflammatory cytokines, including transforming growth factor-β1 and IL-10, were increased in the EPC group. In addition, expression levels of brain-derived neurotrophic factor, vascular endothelial growth factor, and neurotrophic growth factor were increased following transplantation of EPCs. EPC transplantation could improve neurological function of ICH rats. The protective effect may be mediated by promotion of neuroprotective cytokine secretion, restoration of the BBB, reduction of cell death, and the decrease in inflammation.
Highlights
Intracerebral hemorrhage (ICH), which manifests as brain parenchymal bleeding, accounts for approximately 10–20% of cerebral strokes [1]
Neurological function of the animals was compared between the Endothelial progenitor cells (EPCs) and phosphate-buffered saline (PBS) groups before cell transplantation, and there was no significant difference in modified neurological severity score (mNSS) between groups
We measured expression levels of claudin-5 and zonula occluden (ZO)-1 and found that expression of these tight junction proteins decreased after cerebral hemorrhage, which indicated blood–brain barrier (BBB) disruption
Summary
Intracerebral hemorrhage (ICH), which manifests as brain parenchymal bleeding, accounts for approximately 10–20% of cerebral strokes [1]. Patients with ICH usually have poor functional outcomes and high mortality rates. It is considered one of the most devastating diseases [2]. EPCs Attenuate Brain Injury after ICH is no effective neuroprotective treatment currently available [3]. An important key pathophysiological mechanism of neurological deterioration after ICH is perihematomal edema. This is mainly caused by loss of integrity of the blood–brain barrier (BBB) and inflammatory reactions [4, 5]. Reducing brain edema after ICH may be a potentially effective therapeutic method for ICH
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