Abstract
The morbidity, mortality, and disability associated with intraventricular hemorrhage (IVH) secondary to intracerebral hemorrhage (ICH) represent a global burden. To date, there is no effective therapy for ICH other than supportive care. In this study, we assessed the neuroprotective effects of Cattle encephalon glycoside and ignotin (CEGI) injection in a rat model of ICH with ventricular extension (IVH/ICH). The IVH/ICH rat model was induced via injection of type IV collagenase in the caudate nucleus of Sprague-Dawley rats. The experimental animals were randomized to receive CEGI, monosialotetrahexosyl ganglioside (GM-1), or normal saline. The modified Garcia scale, corner turn test, immunofluorescence staining for myelin basic protein (MBP) and microtubule associated protein 2 (MAP-2), transmission electron microscopy (TEM), and magnetic resonance imaging were employed to evaluate the neuroprotective effect of CEGI in the IVH/ICH rat model. CEGI treatment significantly alleviated the neurobehavioral dysfunction, reduced the lateral ventricular enlargement, promoted hematoma absorption, effectively up-regulated MBP/MAP-2 expression, and ameliorated white matter fiber damage post-ICH induction. Our results demonstrate that CEGI has significant neuroprotective effects in a rat model of IVH/ICH. Therefore, it can be used as a candidate drug for the clinical treatment of IVH/ICH.
Highlights
We investigated the efficacy of daily injections of 4 ml/kg CEGI for alleviating the neurological defects associated with Intraventricular hemorrhage (IVH)/Intracerebral hemorrhage (ICH) in a rat model
Injury to axons and the myelin sheath at the subcortical white matter and peri-hematoma persisted for 14 days post-ICH induction
The expression of myelin basic protein (MBP) and microtubule associated protein 2 (MAP-2) in the subcortical white matter was increased at days 7 and 14 post-ICH induction in the ICH +CEGI 4 ml/kg group
Summary
The effect of CEGI treatment on IVH/ICH has not yet been investigated. Carnosine, another active component of CEGI, was reported to have therapeutic activity in cases of ischemic brain damage via the modulation of mitochondrial function and autophagy[12]. These results suggest that CEGI may be beneficial in the treatment and/or prevention of prolonged hydrocephalus secondary to IVH/ICH. The multi-target effects of CEGI were assessed in a rat model of IVH/ICH using white matter lesions as an indicator for treatment progress. We explored the potential effect of CEGI treatment on hydrocephalus after IVH/ICH
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