Acute injury is one of the substantial stage post-traumatic brain injury (TBI) occurring at the moment of impact. Decreased metabolism, unregulated cerebral blood flow and direct tissue damage are triggered by acute injury. Understating the biochemical alterations associated with acute TBI is critical for brain plasticity and recovery. The objective of this study was to investigate the biochemical and molecular changes in hippocampus, corpus callosum and thalamus brain regions post-acute TBI in rats. Fourier Transform Infrared (FTIR) imaging spectroscopy were used to collect chemical images from control and 3 hrs post-TBI (Marmarou model was used for the TBI induction) rat brains and adjacent sections were treated by hematoxylin and eosin (H&E) staining to correlate with the disruption in tissue morphology and injured brain biochemistry. Our results revealed that the total lipid and total protein content decreased significantly in the hippocampus, corpus callosum and thalamus after brain injury. Reduction in lipid acyl chains (-CH₂) associated with an increase in methyl (-CH₃) and unsaturated lipids olefin=CH concentrations is observed. Furthermore, there is a decrease in the lipid order (disorder), which leads to an increase in acyl chain fluidity in injured rats. The results suggest acute TBI damages brain tissues mechanically rather than chemical alterations. This will help in assessing successful therapeutic strategy in order to mitigate tissue damage in acute TBI period.

急性损伤是在发生撞击时发生的实质性创伤后脑损伤（TBI）之一。急性损伤触发新陈代谢下降，大脑血流失调和直接组织损伤。低估与急性TBI相关的生化改变对于大脑可塑性和恢复至关重要。这项研究的目的是调查大鼠急性TBI后海马，call体和丘脑脑区域的生化和分子变化。使用傅里叶变换红外（FTIR）成像光谱从对照和TBI后3小时（Marmarou模型用于TBI诱导）大鼠脑中收集化学图像，并用苏木精和曙红（H＆E）染色处理邻近部分，以与组织形态的破坏和受损的脑生化。我们的结果表明，脑损伤后海马，call体和丘脑中的总脂质和总蛋白含量显着降低。减少脂质酰基链（-CH₂）观察到与甲基（-CH ₃）和不饱和脂质烯烃＝ CH浓度增加有关。此外，脂质顺序（紊乱）减少，导致受伤大鼠的酰基链流动性增加。结果表明，急性TBI会机械损伤脑组织，而不是化学改变。这将有助于评估成功的治疗策略，以减轻急性TBI期的组织损伤。