Mild traumatic brain injuries can have long-term consequences that interfere with the life of the patient and impose a burden on our health care system. Oxidative stress has been identified as a contributing factor for the progression of neurodegeneration following TBI. A major source of oxidative stress for many veterans is cigarette smoking and second-hand smoke, which has been shown to have an effect on TBI recovery. To examine the potential influences of second-hand smoke during recovery from TBI, we utilized a mouse model of closed head injury, followed by repeated exposure to cigarette smoke and treatment with a neuroprotective antioxidant. We found that neither the mild injuries nor the smoke exposure produced axonal damage detectable with amino cupric silver staining. However, complexity in the dendritic arbors was significantly reduced after mild TBI plus smoke exposure. In the hippocampus, there were astrocytic responses, including Cyp2e1 upregulation, after the injury and tobacco smoke insult. This study provides useful context for the importance of lifestyle changes, such as reducing or eliminating cigarette smoking, during recovery from TBI.

轻度创伤性脑损伤可能会产生长期后果，影响患者的生活并给我们的医疗保健系统带来负担。氧化应激已被确定为 TBI 后神经变性进展的促成因素。许多退伍军人的氧化应激的主要来源是吸烟和二手烟，这已被证明对 TBI 恢复有影响。为了检查 TBI 恢复过程中二手烟的潜在影响，我们使用了闭合性头部损伤的小鼠模型，然后反复接触香烟烟雾并使用神经保护性抗氧化剂进行治疗。我们发现轻度损伤和烟雾暴露都不会产生氨基铜银染色可检测到的轴突损伤。然而，轻度 TBI 加烟雾暴露后，树突状乔木的复杂性显着降低。在海马体中，有星形胶质细胞反应，包括 Cyp2e1 在受伤和烟草烟雾侮辱后的上调。这项研究为 TBI 恢复期间改变生活方式的重要性提供了有用的背景，例如减少或消除吸烟。