Enhanced pulmonary inflammation following experimental intracerebral hemorrhage.

P84: Effect of Insulin-Like Growth Factor 2 (IGF2) as a Microglia-Derived Anti-Iinflammatory Ccytokine on Improving Memory Impairment Following Hippocampal Intracerebral Hemorrhage in Rat

Insulin-like growth factor 2 (IGF2) as a microglia-derived anti-inflammatory cytokine has a pivotal activity in memory consolidation. However, there is limited evidence on brain cell-originated IGF2 expression, regulation and function in pathological condition and neuro-inflammation. Hence, the present study was conducted to investigate the effect of IGF2 on improving the memory impairment in a...

Neuroprotection of Botch in experimental intracerebral hemorrhage in rats

Notch1 maturation participates in apoptosis and inflammation following intracerebral hemorrhage (ICH). It has been reported that Botch bound to and blocked Notch1 maturation. Here we estimated the role of Botch in ICH-induced secondary brain injury and underlying mechanisms. Experimental ICH model was induced by autologous arterial blood injection in Sprague-Dawley rats, and cultured primary ra...

Therapeutic Benefit of Intravenous Administration of Human Umbilical Cord Blood- Mononuclear Cells Following Intracerebral Hemorrhage in Rat

Objective(s) Human umbilical cord blood (HUCB) is now considered as a valuable source for stem cell–based therapies. Previous studies showed that intravascular injection of the HUCB significantly improves neurological functional recovery in a rat model of intracerebral hemorrhage (ICH). In the present study, we hypothesize transplanted HUCB derived mononuclear cells (UC-MCs) can decrease injur...

Pulmonary hemorrhage and the management following Russell’s viper (Daboia russelii) envenoming in Sri Lanka

Interleukin-4 Ameliorates the Functional Recovery of Intracerebral Hemorrhage Through the Alternative Activation of Microglia/Macrophage

Neuro-inflammation plays an important role in the recovery of brain injury after stroke. Microglia/macrophage is the major executor in the neuro-inflammation, which can be polarized into two distinct phenotypes: injurious/toxic classical activation (M1 phenotype) and protective alternative activation (M2 phenotype). Here, we investigated whether intracerebral administration of interleukin-4 (IL...