Cinnamon and traumatic brain injury

创伤性脑损伤（TBI）和相关的合并症是导致脑损伤的重要因素。 残疾军人。因此，迫切需要找到一种有效的， 安全和经济的解决方案。轴突损伤是导致 TBI后观察到的行为缺陷。据认为，轴突损伤期间， TBI通过神经炎症和脱髓鞘和/或不能 髓鞘再生肉桂是一种常用的调味料，其代谢产物 苯甲酸钠（NaB）是一种广泛使用的食品防腐剂和FDA批准的药物， 治疗儿童尿素循环障碍和非酮症高甘氨酸血症。在这里， 我们将研究一个令人兴奋的假设，肉桂代谢物NaB结合到 过氧化物酶体增殖物激活受体β配体结合域 （具体目的I）诱导小胶质细胞中的抗炎并促进小胶质细胞的成熟。 OPCs（特异性目的II），在TBI小鼠模型中产生神经保护作用（特异性 目标三）。这一尖端的优点提案的积极成果将把NaB描述为一个 新的无毒的PPARβ配体，增强了减弱小胶质细胞的可能性 激活，促进髓鞘再生和治疗TBI患者的肉桂及其 代谢产物NaB作为主要或辅助治疗。

Traumatic brain jury (TBI) and associated co-morbidities are important contributors of disability among military personnel. Therefore, it is an urgent need to find an effective, a safe and an economical solution for this. Axonal injury is an important contributor to the behavioral deficits observed following TBI. It is believed that axonal injury during TBI is potentiated by neuroinflammation and demyelination and/or failure to remyelination. Cinnamon is a commonly used flavoring material and its metabolite sodium benzoate (NaB) is a widely-used food preservative and a FDA-approved drug for the treatment of urea cycle disorders and non-ketotic hyperglycinemia in children. Here, we will examine an exciting hypothesis that cinnamon metabolite NaB binds to the ligand-binding domain of peroxisome proliferator-activated receptor beta (PPARβ) (Specific aim I) to induce anti-inflammation in microglia and promote maturation of OPCs (Specific aim II), resulting in neuroprotection in a mouse model of TBI (Specific aim III). A positive outcome of this cutting-edge merit proposal will delineate NaB as a new nontoxic ligand of PPARβ and enhance the possibility of attenuating microglial activation, promoting remyelination and treating TBI patients with cinnamon and its metabolite NaB as primary or adjunct therapy.