Aloin Protects Against Blood-Brain Barrier Damage After Traumatic Brain Injury in Mice / 神经科学通报·英文版

Aloin is a small-molecule drug well known for its protective actions in various models of damage. Traumatic brain injury (TBI)-induced cerebral edema from secondary damage caused by disruption of the blood-brain barrier (BBB) often leads to an adverse prognosis. Since the role of aloin in maintaining the integrity of the BBB after TBI remains unclear, we explored the protective effects of aloin on the BBB using in vivo and in vitro TBI models. Adult male C57BL/6 mice underwent controlled cortical impact injury, and mouse brain capillary endothelial bEnd.3 cells underwent biaxial stretch injury, then both received aloin treatment. In the animal experiments, we found 20 mg/kg aloin to be the optimum concentration to decrease cerebral edema, decrease disruption of the BBB, and improve neurobehavioral performance after cortical impact injury. In the cellular studies, the optimum concentration of 40 μg/mL aloin reduced apoptosis and reversed the loss of tight junctions by reducing the reactive oxygen species levels and changes in mitochondrial membrane potential after stretch injury. The mechanisms may be that aloin downregulates the phosphorylation of p38 mitogen-activated protein kinase, the activation of p65 nuclear factor-kappa B, and the ratios of B cell lymphoma (Bcl)-2-associated X protein/Bcl-2 and cleaved caspase-3/caspase-3. We conclude that aloin exhibits these protective effects on the BBB after TBI through its anti-oxidative stress and anti-apoptotic properties in mouse brain capillary endothelial cells. Aloin may thus be a promising therapeutic drug for TBI.

Relationship between trauma-induced coagulopathy and progressive hemorrhagic injury in patients with traumatic brain injury / 中华创伤杂志(英文版)

Progressive hemorrhagic injury (PHI) can be divided into coagulopathy-related PHI and normal coagu- lation PHI. Coagulation disorders after traumatic brain injuries can be included in trauma-induced coagulopathy (TIC). Some studies showed that TIC is associated with PHI and increases the rates of disability and mortality. In this review, we discussed some mechanisms in TIC, which is of great importance in the development of PHI, including tissue factor (TF) hypothesis, protein C pathway and thrombocytopenia. The main mechanism in the relation of TIC to PHI is hypocoagulability. We also reviewed some coagulopathy parameters and proposed some possible risk factors, predictors and therapies.

Risk factors related to hospital mortality in patients with isolated traumatic acute subdural haematoma: analysis of 308 patients undergone surgery / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Acute subdural haematoma (ASDH) is a common traumatic brain injury with a relatively high mortality rate. However, few studies have examined the factors predicting the outcome of isolated traumatic ASDH. This clinical study examined the hospital mortality and analyzed the risk factors for mortality in patients treated surgically for isolated traumatic ASDH.</p><p><b>METHODS</b>We collected 308 consecutive patients who underwent neurosurgery for isolated traumatic ASDH between January 1999 and December 2007 and used multivariate Logistic regression analysis to evaluate the influence of 11 clinical variables on hospital mortality.</p><p><b>RESULTS</b>The overall hospital mortality was 21.75% (67/308). Age (OR = 1.807), preoperative Glasgow Coma Score (OR = 0.316), brain herniation (OR = 2.181) and the time from trauma to decompression (OR = 1.815) were independent predictors of death, while no independent association was observed between hospital mortality and haematoma volume, midline shift, acute brain swelling or brain herniation duration, although these variables were correlated with hospital mortality in univariate analyses.</p><p><b>CONCLUSIONS</b>This study identified the risk factors for hospital mortality in patients who underwent surgical treatment for isolated traumatic ASDH. An increased risk of death occurs in patients who are over 50 years of age and have lower preoperative Glasgow Coma Scores, the presence of brain herniation and a long interval between trauma and decompression. The findings should help clinicians determine management criteria and improve survival.</p>

Increased protein and mRNA expression of endostatin in the ischemic brain tissue of rabbits after middle cerebral artery occlusion / 神经科学通报·英文版

<p><b>OBJECTIVE</b>To explore the changes of endostatin (a strong anti-angiogenesis factor) and vascular endothelial growth factor (VEGF) in the brain tissues of rabbits following cerebral ischemia induced by middle cerebral artery occlusion (MCAO).</p><p><b>METHODS</b>Twenty-four New Zealand white rabbits were randomly divided into 5 groups: control (n = 5), sham-operation (n = 4), 2-hour ischemia (n = 5), 24-hour ischemia (n = 5), and 48-hour ischemia (n = 5). The expression of VEGF and endostatin were measured by enzyme-linked immunosorbent assay (ELISA) and immunohistochemistry, respectively. In situ hybridization was used to characterize the expression of mRNA for the endostatin.</p><p><b>RESULTS</b>Both the protein (at least 50%, P < 0.01) and mRNA (at least 70%, P < 0.05) of endostatin increased significantly in the ischemic brain tissues after MCAO compared with the control group. VEGF increased at least 270% in the brain after cerebral ischemia (P < 0.05).</p><p><b>CONCLUSION</b>Cerebral ischemia leads to an up-regulation of endostatin in the brain, which is not associated with the increase of VEGF in the brain. The increase of endostatin may serve as a deleterious mechanism for ischemic injury through blocking angiogenesis.</p>