创伤性脑损伤（TBI）是全球死亡和残疾的主要原因之一，给TBI患者的生活质量和国家医疗保健系统带来巨大负担。周围器官，尤其是肾脏和肝脏，可能会受到脑组织损伤后分子反应发生的影响。虽然脑外伤后继发性损伤反应已在大脑中得到充分研究，但这些反应对周围器官的影响/后果尚未完全阐明。因此，我们的研究旨在调查这些反应的免疫反应性，特别是通过急性和慢性 TBI 后肾脏和肝脏中的促炎细胞因子和自噬标记物。通过 Marmarou 减重模型对 2 个月大的雌性 Balb/c 小鼠进行实验。在TBI后24小时（急性）和30天（慢性）时采集肝脏和肾脏组织样本，进行组织病理学和免疫反应性分析。与TBI组相比，两个TBI组的男性肝脏和肾脏组织中白细胞介素（IL）-6水平显着升高与对照组相比，但在女性 r-mTBI 慢性肝脏和 r-mTBI 急性肾脏中发现降低。研究发现，肿瘤坏死因子 a (TNF-a) 水平仅在女性 r-mTBI 慢性肾组织和 mTBI 慢性肝组织中增加。男性和女性 r-mTBI 肝组织中 IL-1b 水平升高，但女性 mTBI 肾组织中 IL-1b 水平降低。诱导型一氧化氮合酶（iNOS）水平在女性 mTBI 急性和 r-mTBI 慢性肾组织和 mTBI 肝组织中显着升高，但在 r-mTBI 急性肾和 r-mTBI 肝组织中降低。 Beclin-1 水平在男性 mTBI 慢性和 r-mTBI 急性肝组织中升高，但在 r-mTBI 慢性组中降低。 LC3A/B和P62/SQSTM1水平在女性mTBI慢性和男性r-mTBI慢性肝组织中显着升高，但在男性r-mTBI和女性r-mTBI急性肾组织中降低。在肝脏和肾脏组织中也观察到了显着的组织病理学变化，这些变化取决于 TBI 的严重程度、性别和 TBI 后的时间。结果表明，TBI 可能引起外周分子反应，特别是在炎症细胞因子和 TBI 水平的改变方面。自噬标记物，具有性别和时间依赖性。这表明，在 TBI 后的急性和慢性阶段，TBI 可能在肾脏和肝脏的细胞损伤中发挥重要作用，从而确保 TBI 的影响可能不仅限于大脑。

Traumatic brain injury (TBI) is one of the major causes of death and disability worldwide, and brings a huge burden on the quality of life of patients with TBI and the country's healthcare system. Peripheral organs, especially the kidney, and liver, may be affected by the onset of molecular responses following brain tissue damage. While secondary injury responses post TBI has been well studied in the brain, the effect/consequences of these responses in the peripheral organs have not yet been fully elucidated. Thus, our study aimed to investigate the immunoreactivity of these responses, particularly via proinflammatory cytokines and autophagy markers in the kidney and liver post-acute and chronic TBI.Mild TBI (mTBI) and repetitive mTBI (r-mTBI) were induced in male and female 2-month-old Balb/c mice via the Marmarou weight-drop model. Liver and kidney tissues were sampled at 24 hours (acute) and 30 days (chronic) post TBI and subjected to histopathological and immunoreactivity analysis.Interleukin (IL)-6 levels were significantly increased in the male liver and kidney tissues in both TBI groups compared to the control group but were seen to be decreased in the female r-mTBI chronic liver and r-mTBI acute kidney. Tumor necrosis factor a (TNF-a) levels were found to increase only in the female r-mTBI chronic kidney tissue and mTBI chronic liver tissue. IL-1b levels were increased in the male and female r-mTBI liver tissues but decreased in the female mTBI kidney tissue. Inducible nitric oxide synthase (iNOS) levels were found to be significantly increased in the female mTBI acute and r-mTBI chronic kidney tissue and mTBI liver tissue, but decreased in the r-mTBI acute kidney and r-mTBI liver tissues. Beclin-1 levels were increased in male mTBI chronic and r-mTBI acute liver tissue but decreased in the r-mTBI chronic group. LC3A/B and P62/SQSTM1 levels were significantly increased in the female mTBI chronic and male r-mTBI chronic liver tissues but decreased in the male r-mTBI and female r-mTBI acute kidney tissues. Significant histopathological changes were also observed in the liver and kidney tissue which were dependent on the TBI severity, gender, and time post TBI.The results showed that TBI may elicit peripheral molecular responses, particularly in terms of alteration in the levels of inflammatory cytokines and autophagy markers, which were gender- and time-dependent. This suggests that TBI may have a significant role in the cellular damage of the kidney and liver in both the acute and chronic phases post TBI, thus ensuring that the effects of TBI may not be confined to the brain.