Objective:To investigate the effect of hyperbaric oxygen (HBO) therapy on microglia polarization after traumatic brain injury (TBI) in rats.Methods:A total of 168 8-week-old SD rats were randomly divided into sham operation (SH) group, sham operation+ HBO (SH+ HBO) group, traumatic brain injury (TBI) group, and traumatic brain injury+ HBO (TBI+ HBO) group, with 42 rats in each group. The TBI rat model and sham operation rat model were established. The observation time points of each group were 1 h, 6 h, 12 h, 24 h, 72 h, 7 d and 14 d. The SH+ HBO group and the TBI+ HBO group were treated with HBO. The modified neurological severity score (mNSS) was used to evaluate the recovery of the neurological function in TBI rats. After taking the injured brain tissues from the decapitated rats, the inducible nitric oxide synthase (iNOS), a microglia marker, and chitinase 3-like 3 (YM1) were detected by Western blotting. The expression levels of IL-6 and IL-10 were detected by ELISA.Results:Compared with the TBI group, mNSS in the TBI+ HBO group was decreased significantly at 7 d and 14 d after injury ( P<0.05). Compared with the SH group and the SH+ HBO group, the expression levels of iNOS protein in brain tissues of the TBI group and the TBI+ HBO group were significantly increased at 24 h, 72 h, and 7 d after TBI ( P<0.05). Compared with the TBI group, the expression levels of iNOS protein in brain tissues of the TBI+ HBO group were significantly decreased at 72 h and 7 d after TBI ( P<0.05). Compared with the SH group and the SH+ HBO group, the expression levels of YM1 protein in brain tissues of the TBI group and the TBI+ HBO group were significantly increased at 6 h, 12 h, 24 h, and 72 h after TBI ( P<0.05); compared with the TBI group, the expression levels of YM1 protein in brain tissues of the TBI+ HBO group were significantly increased at 12 h and 24 h after TBI ( P<0.05). Compared with the SH group and the SH+ HBO group, the expression levels of IL-6 in the TBI group and the TBI+ HBO group were increased significantly after TBI ( P<0.05); compared with the TBI group, the expression levels of IL-6 in the TBI+ HBO group were decreased significantly at 24 h, 72 h, and 7 d after TBI ( P<0.05). Compared with the SH group and the SH+ HBO group, the expression levels of IL-10 in the TBI group and the TBI+ HBO group were significantly increased after TBI ( P<0.05); compared with the TBI group, the expression levels of IL-10 in the TBI+ HBO group were significantly increased at 24 h and 72 h after TBI ( P<0.05). Conclusion:HBO treatment can effectively improve the hypoxic-ischemic state in injured brain tissues of TBI rats, promote the restoration of blood-brain barrier, facilitate the repopulating of M2 type microglia, and promote the polarization of microglia from M1 to M2 in the early stage of brain injury.

Background: 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 via promoting the polarization of MG into M2 after TBI. Methods: 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. Results: 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. Conclusions: 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.

Although there are reports of the beneficial effects of hyperbaric oxygen (HBO) therapy in experimental settings, there are few clinical trials of HBO therapy for acute spinal cord injury (SCI). We investigated the effect of HBO in acute SCI by measuring plasma high mobility group box 1 (HMGB1) and nuclear factor kappa-B (NF-kappa B) levels, and by monitoring changes in electromyogram F-persistence (the percentage of discernible F-waves) and F-chronodispersion (the difference between minimal and maximal latency). We enrolled 79 acute SCI patients and randomly divided them into control (conventional treatment) and the treatment (conventional treatment plus HBO therapy) groups. Plasma was collected before treatment and after treatment on 1st, 3rd, 7th, 10th and 30th day for the measurement of HMGB1 and NF-kappa B. Electromyogram F-waves were detected before therapy and after therapy on the 10th and 30th days. Clinical profiles and neurological outcomes were evaluated using American Spinal Injury Association (ASIA) and Frankel Grade scores. Compared to the control group, HBO therapy down-regulated HMGB1 and NF-kappa B expression in patients with acute SCI on days 3, 7, 10 and 30 (p < 0.05). F-wave chronodispersion decreased at days 10 and 30 (p < 0.01) following HBO. ASIA and Frankel Grade motor/pain scores in the treatment group were significantly improved on day 30 (p < 0.01). There was a positive correlation between plasma NF-kappa B at day 7 and F-wave dispersion at day 30 (r = 0.76, p = 0.00). In summary, HBO therapy regulated the inflammatory reaction in secondary SCI by decreasing plasma HMGB1/NF-kappa B levels and reducing the dispersion of electromyogram F-waves of the lower limbs, thereby promoting neurological function recovery.

Beginning at the end of 2019, corona virus disease 2019(COVID-19) caused by sevare acute respiratory syndrome coronavirus(SARS-CoV-2) appeared in Wuhan, China, and spread rapidly across the country. Prior to this, there had been two outbreaks in the world that caused serious consequences by different coronaviruses: severe acute respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome coronavirus (MERS-CoV). This article introduces the structure and classification of coronaviruses, discusses the origin, virological characteristics, and epidemiological overview of three coronaviruses-SARS-CoV, MERS-CoV, and SARS-CoV-2, and reviews the drugs that are currently on the market and are being developed to treat coronavirus infections, in order to explain the characteristics of coronavirus and provide new ideas for the prevention and control of 2019-nCoV and new coronavirus.