ABSTRACT
Objective To investigate the effect of combined application of mannitol and monosialoganglioside on neurological function and its efficacy in brain edema after intracerebral hemorrhage. Methods 92 cases of cerebral edema in patients with cerebral hemorrhage in our hospital, were randomly divided into groups, each group of 46 cases, the control group on the basis of the treatment of mannitol (125mL per times, once per 8h) treatment, the study group on the basic of control group received monosialogangliosides (20mg per times, once daily), 10d for a course of treatment, determination of serum indexes, neurological functions were recorded. Results The effective rate of control group was 71.74%, which was lower than 91.30% of the study group, there was significant difference (P < 0.05); compared with control group after treatment , in study group the intracranial pressure, intracranial hematoma, edema decreased, the urine volume increased, National Institutes of Health Stroke Scale (NIHSS) and quality of life score decreased, interleukin (IL-1β), high sensitive C reaction protein (Hs-CRP), IL-6 and IL-8 levels decreased, Na+-K+-ATP enzyme increased, the ratio of cerebrospinal fluid albumin and serum albumin, matrix metalloproteinase (MMP-2) and MMP-9 decreased, there were significant differences (P < 0.05). Conclusion The effect of the combined application of mannitol and monosialoganglioside on cerebral edema after cerebral hemorrhage is exact and could improve neurologic function.
ABSTRACT
OBJECTIVE: The goal of this study was to investigate the protective effect of recombinant human EPO(rhEPO) on cerebral microvascular endothelial cells and the mechanisms by which rhEPO interacts with TJs proteins, claudin-5, Occludin and ZO-1 during the early period following traumatic brain injury. RESEARCH DESIGN: Rats (n = 81) were randomly divided into sham-operated group, TBI group and rhEPO+TBI group. Traumatic brain injury was induced by the Marmarou method. METHODS AND PROCEDURES: Rats were killed at 3, 24, 72 and 168 hours after TBI. The integrity of the blood-brain barrier was investigated by using a spectrophotometer to assess extravasation of Evans blue dye. The expression of Claudin-5, Occludin and ZO-1 were determined by immunohistochemistry and real-time fluorescence quantitative PCR. RESULTS: From 3 hours to 3 days, rats in the TBI group demonstrated a remarkable increase in Evans blue content in the brain, relative to rats in the sham-operated group (p < 0.05). The expression of Claudin-5 and Occludin was significantly lower than those in the sham-operated group (p < 0.05). In contrast, rats in the TBI+rhEPO group demonstrated a significant decrease in brain levels. CONCLUSION: It was found that administration of rhEPO protected cerebral microvascular endothelial cells and reduced permeability of BBB and the mechanisms may be due to increasing the expression of TJs proteins.
Subject(s)
Brain Injuries, Traumatic/pathology , Brain Injuries, Traumatic/prevention & control , Endothelial Cells/pathology , Erythropoietin/therapeutic use , Tight Junctions/drug effects , Animals , Blood-Brain Barrier/drug effects , Blood-Brain Barrier/physiopathology , Claudin-5/genetics , Claudin-5/metabolism , Disease Models, Animal , Drug Administration Schedule , Gene Expression Regulation/drug effects , Occludin/genetics , Occludin/metabolism , RNA, Messenger , Rats , Rats, Sprague-Dawley , Time Factors , Zonula Occludens-1 Protein/genetics , Zonula Occludens-1 Protein/metabolismABSTRACT
Objective To investigate the functional and ultrastructural changes of cerebral microvascular endothelial cells at early stage following traumatic brain injury (TBI) in rats. Methods The rat models with closed brain injury were established with the improved Marmarous method. The expressions of thrombomodulin (TM) and von Willebrand factor (vWF) were determined by immunohistochemical techniques (5 rats per group) and real-time quantitative RT-PCR (5 rats per group) respectively at 1, 4, 8, 12, 24 hours and at days 3 and 7 after injury. Results TM and vWF started expression at 4 hours, reached peak at 24 hours and recovered to normal at day 7 after TBI. The expression levels of TM and vWF at different time points in sham control group showed statistical difference compared with damage group (P < 0.05). Conclusion The activation of the cerebral microvascular endothelial cells at early stage after TBI is the main mechanism of early secondary brain injury.
