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Study Design: Basic science study investigating the potential molecular mechanisms of hyperbaric oxygen (HBO) therapy in mice with spinal cord injury (SCI)., Objective: We aimed to explore the intrinsic mechanisms of HBO for SCI through the lens of ferroptosis in the subacute phase., Summary of Background Data: HBO has been observed to facilitate the restoration of neurological function subsequent to SCI. Ferroptosis is a distinct cellular death mechanism that can be distinguished from apoptosis, necrosis, and autophagy. However, the precise relationship between these two phenomena remains poorly understood., Methods: We established an SCI model and employed a range of techniques, including behavioral assessments, electron microscopy, immunofluorescence, RT-qPCR, Western blotting (WB), Glutathione (GSH) measurement, and iron assay, to investigate various aspects of HBO therapy on SCI in mice. These included analyzing mitochondrial morphology, neuronal count, GSH levels, iron levels, and the expression of genes (Acyl-CoA synthetase family member-2, Iron-responsive element-binding protein-2) and proteins (Glutathione peroxidase 4; system Xc-light chain) associated with ferroptosis. The study included three groups: Sham-operated, SCI, and HBO. Group comparisons were performed using one-way analysis of variance and one-way repeated measures analysis of variance, followed by Tukey's post hoc test. Statistical significance was set at a P < 0.05., Results: Our findings revealed that HBO therapy significantly enhanced the recovery of lower limb motor function in mice following SCI in the subacute phase. This was accompanied by upregulated expression of GPX4 and system Xc-light chain proteins, elevated GSH levels, increased number of NeuN+ cells, decreased expression of the iron-responsive element-binding protein-2 gene, and reduced iron concentration., Conclusions: Our research suggests that HBO therapy has the potential to be an effective treatment for SCI in the subacute phase by mitigating ferroptosis., Competing Interests: The authors report no conflicts of interest., (Copyright © 2023 Wolters Kluwer Health, Inc. All rights reserved.)

Study Design: A functional, transcriptome, and long noncoding RNAs (lncRNAs) expression analysis in the spinal cord of mice after hyperbaric oxygen (HBO) treatment., Objective: We aimed to explore the mechanism by which HBO treats spinal cord injury (SCI) at the level of lncRNAs., Summary of Background Data: Immense amounts of research have established that HBO treatment promotes the recovery of neurological function after SCI. The mechanism of action remains to be clarified., Methods: High-throughput RNA sequencing, Gene Ontology, and Kyoto Encyclopedia of Genes and Genomes enrichment analysis were used to profile lncRNA expression and analyze biological function in the spinal cords of mice from sham-operated, SCI, and HBO-treated groups. The differential expression of lncRNA between the groups was assessed using real-time quantitative polymerase chain reaction., Results: Differential expression across 577 lncRNAs was identified among the three groups. GO analysis showed that free ubiquitin chain polymerization, ubiquitin homeostasis, DNA replication, synthesis of RNA primer, single-stranded telomeric DNA binding, and alpha-amylase activity were significantly enriched. Kyoto Encyclopedia of Genes and Genomes enrichment analysis displayed that vitamin B6 metabolism, one carbon pool by folate, DNA replication, lysine degradation, beta-alanine metabolism, fanconi anemia pathway, and Notch signal pathway were the main pathways with enrichment significance. LncRNAs NONMMUT 092674.1, NONMMUT042986.2, and NONMMUT018850.2 showed significantly different expression between the SCI and the other two groups (P<0.05, <0.01)., Conclusions: This study is the first to determine the expression profiles of lncRNAs in the injured spinal cord after HBO treatment. We identified several important dysregulated lncRNAs in this setting. These results help us better understand the mechanism by which HBO treats SCI and provide new potential therapeutic targets for SCI., Competing Interests: The authors report no conflicts of interest., (Copyright © 2022 Wolters Kluwer Health, Inc. All rights reserved.)

Disruption of the intestinal epithelial barrier following spinal cord injury (SCI) seriously affect long-term quality of life. Oxidative stress-induced epithelial cells' injury contributes to the epithelial barrier dysfunction. Hyperbaric oxygen (HBO) treatment has been proved to alleviate SCI. However, it is unclear whether or not HBO treatment affects intestinal barrier function following SCI. In this study, our purpose was to explore the impact of HBO treatment on intestinal epithelial barrier function and underlying mechanisms following SCI. An SCI model was established in rats, and the rats received HBO treatment. Intestinal injury, mucosal permeability, intercellular junction proteins, and oxidative stress indicators were evaluated in our study. We found that HBO treatment significantly alleviated intestinal histological damage, reduced mucosal permeability, and markedly prevented bacterial translocation. Furthermore, HBO treatment significantly increased the expression of Claudin-1 and E-cadherin, inhibited intestinal tissue oxidative stress as demonstrated by upregulation of superoxide dismutase and glutathione, and HBO downregulated malondialdehyde. Mechanically, we demonstrated that HBO treatment ameliorated intestinal oxidative stress possibly through upregulating nuclear factor E2-related factor 2 (Nrf2) and its downstream targets, Heme oxygenase-1(HO-1), NADH-quinone oxidoreductase-1(NQO-1), and glutamate cysteine ligase catalytic subunit (GCLC). These results suggested that HBO treatment triggered antioxidative effects against intestinal epithelial barrier dysfunction by promoting Nrf2 signaling pathway after SCI.

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-κB) 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-κB. 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-κB 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-κB 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-κB levels and reducing the dispersion of electromyogram F-waves of the lower limbs, thereby promoting neurological function recovery., (Copyright © 2018 Elsevier B.V. All rights reserved.)

Background: Hyperbaric oxygen therapy (HBOT) has been widely used in the clinical setting. In this study, HBOT therapy was evaluated for its ability to ameliorate the epithelial-to-mesenchymal transition (EMT) phenomenon in keloid tissue., Methods: Keloid patients were randomly divided into two groups: keloid patients (K group, 9 patients) and keloid patients receiving HBOT (O group, 9 patients). A third group with normal skin (S group, 9 patients) was established for control. Before HBOT and surgery, a laser Doppler flowmeter was used to measure the keloid blood supply of patients in the O group. Hematoxylin and eosin (H&E) staining was used to observe morphology. E-cadherin, ZO-1, vimentin, fibronectin, vascular endothelial growth factor (VEGF), and hypoxia inducible factor (HIF)-1α were measured by immunofluorescence staining and Western blot analysis. Real-time quantitative polymerase chain reaction (RT-qPCR) was used to evaluate the mRNA expression level of these factors as well., Results: In the O group, keloid blood perfusion was significantly reduced after patients received HBOT. Compared with the K group, lower expression levels of vimentin, vibronectin, VEGF, and HIF-1α were observed in the O group, whereas the expression of E-cadherin and ZO-1 was significantly higher. The mRNA expression of E-cadherin and ZO-1 was also increased after HBOT., Conclusions: The expression levels of factors related to the EMT phenomenon were significantly reversed in keloid patients after they received HBOT, indicating that HBOT may be an effective therapy against the EMT phenomenon in keloid patients.

The inflammatory response is an important source of secondary damage to neuronal tissue in the spinal cord following spinal cord injury (SCI). Hyperbaric oxygen (HBO) therapy reduces inflammation and promotes the restoration of locomotor function following SCI, however, the mechanisms underlying this effect remain to be determined. The aim of the current study was to investigate the mechanisms by which HBO therapy promotes recovery in a rat model of SCI by measuring expression levels of receptor for advanced glycation end products (RAGE) and monocyte chemoattractant protein‑1 (MCP‑1) in spinal cord tissue. Experimental animals (n=90) were divided into three groups: Sham‑operated (SH), SCI (T‑10 laminectomy) and SCI + HBO. Each group was further divided into five subgroups (n=6) that were examined at 12 h, and at 1, 3, 7 and 14 days post‑injury. Recovery of locomotor function was evaluated using the Basso, Beattie and Bresnahan (BBB) scoring system. Neutrophil infiltration was analyzed using myeloperoxidase (MPO) activity assays. The expression of RAGE and MCP‑1 was measured by immunohistochemistry, reverse transcription‑quantitative polymerase chain reaction and western blotting. RAGE and MCP‑1 expression and MPO activity were higher in the SCI groups than in the SH groups at each time point. HBO therapy reduced RAGE and MCP‑1 expression and MPO activity compared with untreated, injured animals at early post‑injury stages. In addition, HBO therapy improved BBB scores at post‑operative day 7 and 14. HBO therapy was, therefore, demonstrated to relieve secondary inflammatory responses, potentially by inhibiting the expression of RAGE and MCP‑1, resulting in significant recovery of locomotor function. The results of the present study may, therefore, be useful in improving the clinical application of HBO therapy for patients with SCI.

Study Design: Experimental animal study of treatment of SCI., Objective: To explore whether HBO treatment protects against secondary SCI by inhibiting the ER stress response., Summary of Background Data: SCI is a neurological disorder that can severely limit the execution of the simplest day-to-day functions. ER stress plays an important role in the induction of neuronal apoptosis after SCI. HBO treatment can alleviate secondary injury and benefit neurological recovery after SCI, but the effect of HBO on ER stress response after SCI is yet to be characterized., Methods: The spinal cord of rats was injured via T10 laminectomy. Experimental animals were randomly assigned to 1 of 3 groups: sham-operated, SCI, and SCI+HBO. Each group was analyzed 1, 2, 3, 7, and 14 days after injury. Neurological recovery was evaluated using the Basso-Beattie-Bresnahan (BBB) scoring system and the TdT-mediated dUTP nick-end labeling reaction was carried out to visualize apoptotic cells. The expression of ER stress-related factors was evaluated by immunohistochemical, western blot, and real-time reverse transcription-polymerase chain reaction analyses., Results: SCI-induced apoptosis and an increase in the levels of CCAAT-enhancer-binding protein homologous protein (CHOP), and caspase-12 and caspase-3 compared with the sham-operated group. HBO treatment decreased CHOP and caspase-12 and caspase-3 expression as well as apoptosis compared with the SCI group. In addition, BBB scores were improved in the SCI+HBO relative to the SCI group at 7 and 14 days., Conclusion: These results suggest that HBO treatment alleviates secondary injury to the spinal cord by inhibiting ER stress induced apoptosis, thereby promoting the recovery of neurological function., Level of Evidence: N/A.

The clinical application of hyperbaric oxygen therapy (HBOT) in spinal cord injury (SCI) has been reported, however the mechanism underlying its therapeutic effects remains to be elucidated. In the present study, SCI was modeled in male Sprague‑Dawley rats. A total of 120 rats were randomly divided into four groups: Sham‑operated group (SH); sham‑operated and hyperbaric oxygen group (SH+HBO); spinal cord injury group (SCI) and spinal cord injury and hyperbaric oxygen treatment group (SCI+HBO). The rats in each group were randomly divided into five smaller groups (12 h, 1, 3, 7 and 14 days after surgery). The mRNA and protein expression levels of NACHT domain‑, leucine‑rich‑repeat‑ and pyrin domain‑containing protein 3 (NALP3) inflammasome, including NALP3, adaptor molecule apoptosis‑associated speck‑like protein (ASC) and caspase‑1 were determined at several time points following injury. The results of the present study demonstrated that HBOT compromised the mRNA and protein expression levels of NALP3, ASC and caspase‑1 in the SCI model rats and HBOT mitigated SCI‑induced interleukin 1β release in the injured spinal cord tissue. It was concluded that HBOT is an effective approach, which can prevent against spinal cord injury, likely by inactivating NALP3 inflammasome.

To determine whether Hyperbaric oxygen preconditioning (HBO-PC) promotes neovascularization by increasing Stromal cell derived factor-1 (SDF-1) and CXC chemokine receptor 4 (CXCR4) in transplanted skin flaps of rats. The epigastric pedicle skin flap was established in a rat model. Rats were randomly assigned to the following five groups: 1) sham-operated group (SH); 2) ischemia followed by reperfusion 3 days postoperatively group (IR3d); 3) ischemia followed by reperfusion 5 days postoperatively group (IR5d); 4) hyperbaric oxygen preconditioning and ischemia followed by reperfusion 3 days postoperatively group (HBO-PC3d); and 5) hyperbaric oxygen preconditioning and ischemia followed by reperfusion 5 days postoperatively group(HBO-PC5d). For the groups receiving HBO-PC, animals underwent 1 hour of HBO at 2.0 ATA in 100% O2 twice per day for 3 days consecutively prior to surgery. After perfusion, Laser Doppler perfusion imaging (LDPI) was performed, and skin flap tissue samples were harvested for histological evaluation and western blot analysis. Perfusion was significantly improved in the HBO-PC groups compared with the IR groups on postoperative 3 and 5. Microvessel density (MVD) was significantly increased by HBO-PC compared with IR groups postoperatively. Western blot analysis revealed that SDF-1 and CXCR4 expression in the HBO-PC groups was significantly increased compared with IR groups. HBO-PC promoted neovascularization via increasing expression levels of SDF-1 and CXCR4 in transplanted skin flaps of rats.

Spinal cord injury (SCI) is a serious medical problem with high mortality and disability rates. Hyperbaric oxygen (HBO) treatment is beneficial for neurological recovery after SCI, but the underlying mechanisms await characterization. This study examined whether HBO treatment following SCI in rats exerts a neuroprotective effect through activation of the toll-like receptor (TLR) 2/nuclear factor (NF)-κB signaling pathway. The SC of rats was injured via T10 laminectomy. Experimental animals (n=144) were divided into four groups: sham-operated (SH), SH+HBO, SCI, and SCI+HBO. Each group was subdivided into six subgroups (n=6 per group) that were examined at 12 h, and 1, 2, 3, 7, and 14 days post-injury. Functional recovery in the hind limb was evaluated using the Basso, Beattie, and Bresnahan (BBB) scoring system. The expression of TLR2 and NF-кB was assessed by real-time polymerase chain reaction and Western blotting, while interleukin-1 (IL)-1β and tumor necrosis factor (TNF)-α levels were measured by enzyme-linked immunosorbent assay. TLR2 and NF-кB levels and histological scores were higher in the SCI than in the SH and SH+HBO groups at various time points. HBO treatment decreased TLR2 and NF-кB expression and histological scores as well as IL-1β and TNF-α levels compared to the SCI group at early post-injury stages. In addition, BBB scores were improved in the SCI+HBO relative to the SCI group at 7 and 14 days. HBO treatment may mitigate secondary injury to the SC by inhibiting inflammatory responses induced by TLR2/NF-кB signaling, thereby promoting functional recovery and improving neurological outcome.

Background Context: Spinal cord injury (SCI) is a serious health issue that may result in high health care costs, with additional social and psychological burdens. Hyperbaric oxygen (HBO) treatment has been found to be beneficial for neurological recovery; however, the underlying mechanisms are yet to be characterized., Purpose: The aim of this study was to investigate the mechanisms of HBO treatment in SCI by measuring the expression levels of vascular endothelial growth factor (VEGF) and Connexin43 (CX43) in the injured spinal cord tissue., Study Design/setting: An experiment animal study of rats undergoing SCI and HBO treatment., Methods: The spinal cord injury model was established in rats, which were randomly divided into the following four groups: (1) the sham-operated group (SH), (2) the sham-operated and hyperbaric oxygen treatment group (SH+HBO), (3) the spinal cord injury group (SCI), and (4) the spinal cord injury and hyperbaric oxygen treatment group (SCI+HBO). For groups of SH+HBO and SCI+HBO, the animals received 1 hour of HBO at 2.0 ATA in 100% O2 twice per day for 3 days and then daily for the following days consecutively after surgery. After operation, neurological assessments were performed, the spinal cord tissue samples were harvested for histopathological evaluation, Western blot and real-time polymerase chain reaction analysis., Results: The Basso-Bettie-Bresnahan scores were significantly improved in the SCI+HBO group compared with the SCI group on the postoperative 7th and 14th days. The histology scores were significantly decreased by HBO treatment compared with that in the SCI group on the postoperative 3rd, 7th, and 14th days. Western blot analysis and real-time polymerase chain reaction revealed that the expression level of vascular endothelial growth factor (VEGF) in the SCI+HBO group was significantly increased compared with the SCI group. The protein expression level of CX43 and its mRNA level in the SCI+HBO group were significantly decreased on the postoperative 3rd and 7th days, whereas its expression was significantly increased by HBO treatment on the postoperative 14th day compared with the SCI group., Conclusions: HBO treatment improved neurological recovery when applied after SCI. The expression level changes of VEGF and CX43 may contribute to the further understanding on the molecular mechanisms of HBO treatment on SCI., (Copyright © 2014 Elsevier Inc. All rights reserved.)

Study Design: We presented an insight into the effect of hyperbaric oxygen (HBO) on spinal cord injury (SCI), aiming to uncover the dynamics of high-mobility group protein B1 (HMGB1) and nuclear factor κB (NF-κB) after HBO intervention in rats with acute SCI., Objective: Prognosis of SCI is directly linked with the control of secondary injury, in which the inflammatory response plays a leading role. HBO therapy can reduce this secondary damage to the spinal cord. We used an animal model to characterize the therapeutic effect of HBO on SCI., Summary of Background Data: A growing number of studies have confirmed that HBO has gradually become an indispensable element after SCI in reducing neurological disorders, and improving the physical function and quality of life of patients. The role of HBO in the process of HMGB1/NF-κB-related secondary inflammatory responses in SCI has yet to be characterized., Methods: Rats were randomly categorized into sham, sham + HBO, SCI, and SCI + HBO groups. The expression levels of HMGB1 and NF-κB were measured at days 1, 3, 7, and 14 after SCI., Results: After SCI, significant increases in mRNA and protein expression were observed for both HMGB1 and NF-κB (P< 0.01) compared with sham group. HMGB1 mRNA and protein expression levels were decreased after HBO intervention. The decreases were significant at days 7 and 14 (P< 0.05) post-HBO. In the SCI + HBO group, the significant decreases in NF-κB mRNA and protein expression levels were also observed at days 3, 7, and 14 (P< 0.05). After HBO intervention, a significant increase was seen in the Basso, Beattie, and Bresnahan score at days 7 and 14 (P< 0.05)., Conclusion: HBO intervention may reduce the secondary damage of SCI caused by inflammatory responses via downregulating the expression of HMGB1/NF-κB, and promoting the repair of neurological function., Level of Evidence: N/A.

Objective. Hyperbaric oxygen therapy (HBOT) has been recommended for the initial and salvage treatment of patients with idiopathic sudden sensorineural hearing loss (ISSHL), but its underlying mechanisms remain unclear. In this study, we investigated whether HBOT alters serum levels of insulin-like growth factor 1 (IGF-1) and heat shock protein 70 (HSP70) in patients with ISSHL. Then, we identified the relationship between hearing recovery and changes in serum IGF-1 and HSP70 levels. Methods. Moderately severe to profound unilateral ISSHL patients (n = 70) and healthy control participants (n = 30) were enrolled. The ISSHL patients were randomly assigned to receive medical therapy alone (MT group, n = 35) or both HBOT and medical therapy (HBOT + MT group, n = 35). Audiometric testing was performed before and after treatment. Serum IGF-1 and HSP70 levels were assessed by ELISA in ISSHL patients pre-and posttreatment and healthy controls. Results. Before treatment, compared with the healthy controls, serum IGF-1 and HSP70 were lower in ISSHL patients. After treatment, serum IGF-1 and HSP70 increased in both the HBOT + MT and MT groups, although they were significantly higher in the HBOT + MT group (p < 0.01). In the HBOT + MT group, these increases were associated with hearing gains. In addition, IGF-1 was strongly associated with HSP70 (r = 0.621, p = 0.001). No such association was found in the MT group (p = 0.757). Conclusion. Administering HBOT in addition to medical therapy can improve the hearing of patients with moderately severe to profound unilateral ISSHL. The improvement is related to the upregulation of IGF-1 and HSP70. [ABSTRACT FROM AUTHOR]

Background: β2-microglobulin has been showing to be vital that associated with brain function and neurological diseases. This study aimed to explore the expressions of β2-microglobulin in blood and urine of the patients with brain injury, and the effect of hyperbaric oxygen therapy on the content of β2-microglobulin.Methods: This prospective study included 54 patients with brain injury and 11 healthy controls. The patients were further assigned to two groups: the conscious disturbance group (n = 32) and the non-conscious disturbance group (n = 22) depending on the Glasgow Coma Scale (GCS). The patients received routine treatment and two courses of hyperbaric oxygen therapy (2.0ATA, 60 min, once a day, 10 days for a course). In the brain injury group, blood β2-microglobulin (β2MG) and urine β2-microglobulin (β2MU) were detected respectively before and after hyperbaric oxygen therapy (HBOT). Consciousness and cognitive scores were performed, correspondingly.Results: Compared with those of the control group, levels of β2MG and β2MU in the brain injury group were significantly increased before HBOT (P < 0.05). Whether it was before or after HBOT, β2MG's content in the conscious disturbance group was higher than that in the non-conscious disturbance group, while β2MU's content was obviously higher than that of the non-conscious disturbance group only before HBOT (P < 0.05). Besides, the β2MU's content in the conscious disturbance group was negatively correlated with GCS score (R = -0.351, P < 0.05) and β2MG's content in the non-conscious disturbance group was positively correlated with the MMSE score grade (R = 0.598, P < 0.05). The ROC curve was used to assess the evaluation of β2MG and β2MU for patients with impaired consciousness with the area under the curve (AUC) of β2MG and β2MU were 0.775 and 0.796, respectively.Conclusion: The concentrations of blood β2-microglobulin and urinary β2-microglobulin were significantly increased in patients with brain injury. The concentrations of β2-microglobulin were correlated with the degree of consciousness and cognitive function. The changes tendency of β2-microglobulin may be considered as clinical monitoring index to evaluate the patient's disturbance of consciousness and cognitive degree, and provide a basis for early assessment of prognosis. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Hyperbaric Oxygen Therapy (HBOT) has definitive therapeutic effects on spinal cord injury (SCI), but its mechanism of action is still unclear. Here, we've conducted a systemic proteomic analysis to identify differentially expressed proteins (DEPs) between SCI rats and HBOT + SCI rats. The function clustering analysis showed that the top enriched pathways of DEPs include oxygen transport activity, oxygen binding, and regulation of T cell proliferation. The results of functional and signal pathway analyses indicated that metabolic pathways, thermogenesis, LXR/RXR activation, acute phase response signaling, and the intrinsic prothrombin pathway in the SCI + HBOT group was higher than SCI group. [ABSTRACT FROM AUTHOR]

Objective: To investigate the therapeutic roles of hyperbaric oxygen exposure on high-altitude pulmonary edema and to determine whether aquaporin-1 and aquaporin-5 were involved in the pathogenesis of HAPE in rats. Methods: Rats were divided into 5 groups: The control group, the HAPE group (HAPE model), the HBO group (hyperbaric oxygen exposure), the NBO group (normobaric oxygen exposure), and the NA group (normal air exposure). Western blot and real-time PCR were used to analyze the pulmonary expressions of AQP1 and AQP5. The wet-to-dry (W/D) weight ratio and the morphology of the lung were also examined. Results: The lung W/D weight ratio in the HAPE group was increased compared with the control group. The injury score in the HBO group was noticeably lower than that in the control group. The mRNA and proteins expressions of AQP1 and AQP5 were significantly downregulated in the HAPE group. Conclusions: Oxygen exposure alleviated high-altitude hypobaric hypoxia-induced lung injury in rats. Additionally, HBO therapy had significant advantage on interstitial HAPE. [ABSTRACT FROM AUTHOR]

Study Design: Experimental animal study of treatment of SCI.Objective: To explore whether HBO treatment protects against secondary SCI by inhibiting the ER stress response.Summary Of Background Data: SCI is a neurological disorder that can severely limit the execution of the simplest day-to-day functions. ER stress plays an important role in the induction of neuronal apoptosis after SCI. HBO treatment can alleviate secondary injury and benefit neurological recovery after SCI, but the effect of HBO on ER stress response after SCI is yet to be characterized.Methods: The spinal cord of rats was injured via T10 laminectomy. Experimental animals were randomly assigned to 1 of 3 groups: sham-operated, SCI, and SCI+HBO. Each group was analyzed 1, 2, 3, 7, and 14 days after injury. Neurological recovery was evaluated using the Basso-Beattie-Bresnahan (BBB) scoring system and the TdT-mediated dUTP nick-end labeling reaction was carried out to visualize apoptotic cells. The expression of ER stress-related factors was evaluated by immunohistochemical, western blot, and real-time reverse transcription-polymerase chain reaction analyses.Results: SCI-induced apoptosis and an increase in the levels of CCAAT-enhancer-binding protein homologous protein (CHOP), and caspase-12 and caspase-3 compared with the sham-operated group. HBO treatment decreased CHOP and caspase-12 and caspase-3 expression as well as apoptosis compared with the SCI group. In addition, BBB scores were improved in the SCI+HBO relative to the SCI group at 7 and 14 days.Conclusion: These results suggest that HBO treatment alleviates secondary injury to the spinal cord by inhibiting ER stress induced apoptosis, thereby promoting the recovery of neurological function.Level Of Evidence: N/A. [ABSTRACT FROM AUTHOR]