Cinnamon and traumatic brain injury

创伤性脑损伤(TBI)及相关并发症是导致脑损伤的重要因素。 军事人员中的残疾。因此，迫切需要找到一种有效的、一种 这是一个安全和经济的解决方案。轴突损伤是导致 脑损伤后观察到的行为缺陷。据认为，轴突损伤在 神经炎症和脱髓鞘和/或未能 重新髓鞘形成。肉桂是一种常用的调味料及其代谢物 苯甲酸钠(NAB)是一种广泛使用的食品防腐剂，也是FDA批准的药物 儿童尿素循环障碍和非酮症高血糖的治疗。这里, 我们将检验一个令人兴奋的假设，即肉桂代谢物NAB与 过氧化物酶体增殖物激活受体β的配体结合域 (特定目的I)诱导小胶质细胞抗炎，促进小胶质细胞成熟 OPC(特异性目标II)，导致脑外伤小鼠模型的神经保护(特异性 目标III)。这一尖端优点提案的积极结果将把NAB描绘成 新的PPARβ无毒配基及增强其抑制小胶质细胞的可能性 肉桂及其制剂活化、促进髓鞘再生和治疗颅脑损伤 代谢物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.