Liang Fang, Kang Nan, Li Pinpin, Liu Xuehua, Li Ge, Yang Jing
Department of Hyperbaric Oxygen, Beijing Chao-Yang Hospital, Capital Medical University, Beijing, China.
Department of Orthopedics, Beijing Chao-Yang Hospital, Capital Medical University, Beijing, China.
Front Neurol. 2021 Jun 3;12:640816. doi: 10.3389/fneur.2021.640816. eCollection 2021.
The neurological defect caused by secondary damage following traumatic brain injury (TBI) is considered critical for the management of TBI. Microglia (MG) are a resident brain macrophage that could differentiate into M1 type or M2 type in response to injury and repair. It is known that the MG transition from M1 phenotype to anti-inflammatory M2 phenotype might reduce secondary injury of TBI. So, a TBI animal model was established and we compared biomarkers of M1 and M2MG between the controls and experimental animals receiving hyperbaric oxygen therapy (HBOT). This study aimed to explore whether HBOT was an effective method to improve neural functional recovery promoting the polarization of MG into M2 after TBI. The rats were randomly divided into four groups: SH (Sham-operated), SH + HBO (hyperbaric oxygen), TBI, and TBI + HBO. Each group included 42 rats, and each of these were divided into the following groups: 1, 6, 12, 24, 72 h, 7, and 14 days. The expression of M1 biomarker inducible nitric oxide synthase (iNOS), M2 biomarker arginase 1 (Arg1), associated cytokine tumor necrosis factor-α (TNF-α), and transforming growth factor-β1 (TGF-β1) was evaluated after the observation time. TBI significantly increased the expression levels of M1 marker iNOS and M2 markers Arg1 at different time points. The increased expression of iNOS was suppressed, while the expression level of Arg1 was enhanced by HBOT. Moreover, HBOT suppressed the pro-inflammatory TNF-α secreted by M1, and promoting the anti-inflammatory TGF-1β. In the present study, HBOT showed the effects on shift of M1 toward M2 phenotype with increased expression of M2 biomarkers and decreased expression of M1 biomarkers in the early stage after TBI.
创伤性脑损伤（TBI）后继发性损伤所导致的神经功能缺损被认为是TBI治疗中的关键问题。小胶质细胞（MG）是脑内固有的巨噬细胞，可在损伤和修复过程中分化为M1型或M2型。已知MG从M1表型向抗炎性M2表型的转变可能会减轻TBI的继发性损伤。因此，建立了TBI动物模型，并比较了对照组与接受高压氧治疗（HBOT）的实验动物之间M1和M2型MG的生物标志物。本研究旨在探讨HBOT是否是一种有效的方法，可通过促进TBI后MG向M2型极化来改善神经功能恢复。大鼠被随机分为四组：假手术组（SH）、假手术+高压氧组（SH + HBO）、TBI组和TBI + HBO组。每组包括42只大鼠，且每组又被分为以下亚组：1、6、12、24、72小时、7天和14天。在观察时间结束后，评估M1生物标志物诱导型一氧化氮合酶（iNOS）、M2生物标志物精氨酸酶1（Arg1）、相关细胞因子肿瘤坏死因子-α（TNF-α）和转化生长因子-β1（TGF-β1）的表达。TBI在不同时间点显著增加了M1标志物iNOS和M2标志物Arg1的表达水平。HBOT抑制了iNOS表达的增加，同时增强了Arg1的表达水平。此外，HBOT抑制了M1分泌的促炎性TNF-α，并促进了抗炎性TGF-1β的分泌。在本研究中，HBOT显示出在TBI早期使M1向M2表型转变的作用，M2生物标志物表达增加，M1生物标志物表达减少。
