高压氧疗法对创伤性脑损伤大鼠氧化应激指标及促／抗炎细胞因子水平的影响

目的：研究高压氧（HBO）疗法对创伤性脑损伤（TBI）大鼠氧化应激指标及促／抗炎细胞因子水平的影响方法：SD雄性大鼠18只,随机分为3组（n=6）：假手术组、损伤对照组和HBO治疗组采用Feency法建立大鼠TBI模型,假手术组只开放骨面,不予打击HBO治疗组大鼠于脑损伤后6h采用动物高压舱,以3ATA压力纯氧治疗60min。所有动物于手术后24h处死,分离脑组织,取伤侧脑半球行组织匀浆,分别测定匀浆上清液中超氧化物歧化酶（SOD）、丙二醛（MDA）、NO的含量以及促炎细胞因子TNF-α、IL-6、IL-1β及抗炎细胞因子IL-10的水平,结果：与损伤对照组相比,HBO治疗使SOD、NO以及IL-10水平升高,同时降低脑内MDA及TNF-α、IL-6、IL-1β的含量结论：HBO治疗可抑制TBI后自由基的生成,从而减轻脂质过氧化反应;同时,HBO治疗可减少促炎细胞因子的生成,促进抗炎细胞因子的产生,从而可减轻损伤脑组织的炎症反应,有助于减轻TBI后脑组织的继发性损伤.     

早期介入高压氧提高寒冷应激下小鼠存活率并促进创面愈合的研究

暴露于寒冷环境下的皮肤开放性伤口是一种高度危险的战场创伤,威胁在室外作业的人员健康。紧急治疗中,高压氧(hyperbaric oxygen, HBO)治疗已经证实能够安全有效地促进皮肤伤口愈合。然而,HBO治疗的最佳干预时间说法仍然并不统一。使用冷应激下的小鼠背部皮肤全层缺损创面模型,比较了HBO治疗的3种干预策略,即分别为创伤后0、24和48 h介入HBO。结果显示,创后立即实施高压氧治疗(0-hHBO组)降低死亡率的效果最佳,小鼠死亡率为33%,而对照组死亡率为100%,且0-hHBO组创面愈合率第5天已达到85%。进一步的血常规和组织免疫化学检测显示,0-hHBO治疗组改善了血液指标,并发挥了一定的抗凋亡作用,这种作用尤其在表皮干细胞中更为明显。因此,研究结果将为HBO的临床应用提供重要的实验数据和线索。     

Hyperbaric biofilms on engineering surfaces formed in the deep sea

Biofouling is a major problem for long-term deployment of sensors in the marine environment. This study showed that significant biofilm formation occurred on a variety of artificial materials (glass, copper, Delrin^? and poly-methyl methacrylate [PMMA]) deployed for 10?days at a depth of 4700?m in the Cayman Trough. Biofilm surface coverage was used as an indicator of biomass. The lowest biofilm coverage was on copper and PMMA. Molecular analyses indicated that bacteria dominated the biofilms found on copper, Delrin^? and PMMA with 75, 55 and 73% coverage, respectively. Archea (66%) were dominant on the glass surface simulating interior sensor conditions, whereas Eukarya comprised the highest percentage of microflora (75%) on the glass simulating the exterior of sensors. Analysis of Denaturing Gradient Gel Electrophoresis profiles indicated that copper and Delrin^? shared the same community diversity, which was not the case for glass and PMMA, or between PMMA and copper/Delrin^?. Sequence alignment matches belonged exclusively to uncultivable microorganisms, most of which were not further classified. One extracted sequence found on glass was associated with Cowellia sp., while another extracted from the PMMA surface was associated with a bacterium in the Alterominidaceae, both γ-proteobacteria. The results demonstrate the necessity of understanding biofilm formation in the deep sea and the potential need for mitigation strategies for any kind of long-term deployment of remote sensors in the marine environment.     

Influence of hyperbaric oxygen therapy on bone metabolism in patients with neoplasm

BackgroundHyperbaric oxygen therapy (HBOT) is useful in the treatment of complications due to radiotherapy in patients with neoplasm. Its effects on bone metabolism are unclear. In our study, we analyzed the effects of HBOT on bone remodeling in oncological patients with radiotherapy.Materials and methodsProspective clinical study in 23 patients with neoplasms undergoing treatment with HBOT due to complications of radiotherapy (hemorrhagic cystitis, proctitis or radionecrosis) and 25 patients with chronic anal fissure. The average number of HBOT sessions was 20 ± 5 (100% oxygen, 2.3 atmospheres and 90 min per day). Serum levels of aminoterminal propeptide of type I collagen (P1NP), C terminal telopeptide of type I collagen (CTX), alkaline phosphatase (AP), 25hydroxyvitamin D (25-OHD), parathyroid hormone (PTH), were measured at 3 time points: T0 (before beginning HBOT), T1 (at the end of HBOT) and T2 (6 months after HBOT).ResultsAt baseline, the patients with neoplasm have higher bone turnover than those with anal fissure. These differences were 41% in CTX (0.238 ± 0.202 ng/mL in neoplasm and 0.141 ± 0.116 ng/mL in fissure; p = 0.04), 30% for PTH (46 ± 36 pg/mL in neoplasm and 32 ± 17 pg/mL in fissure; p = 0.04) and 15% for alkaline phosphatase (80 ± 24 U/L in neoplasm and 68 ± 16 U/L in fissure; p = 0.04). In the group with neoplasm, the values of P1NP decreased 6% after HBOT (T0: 49 ± 31 ng/mL, T2: 46 ± 12 ng/mL; p = 0.03). Also, there were non-significant decreases in PTH (−34%) and CTX (−30%).ConclusionsPatients with neoplasm and complications with radiotherapy have an increase in bone remodeling that may be diminished after HBOT.     

高压氧暴露大鼠肺组织内PPAR通路分子变化规律

目的:研究高压氧暴露大鼠肺组织内过氧化物酶体增殖因子活化受体(PPAR)通路分子表达变化规律。方法:27只雄性SD大鼠随机分为高压常氧对照组(0.23 MPa空气)、高压氧时间序列处理组(0.23 MPa纯氧,分别暴露2 h、4 h、6 h和8 h),持续小流量通风,维持舱内O2浓度>99%。应用HE染色观察各组大鼠肺组织形态学变化;应用oligo芯片检测各个时间表达谱;应用RT-PCR验证发生改变的部分PPAR通路基因。结果:与高压常氧对照组相比,高压氧时间序列处理组造成的肺损伤逐渐加重;表达谱芯片的基因本体论(Go)富集分析结果中有一类PPAR通路类,包含有多个PPAR通路分子;RT-PCR结果提示PPARδ-和PPARγ-均在较长时间高压氧暴露的肺组织中上调。结论:高压氧长时间暴露造成的肺型氧中毒可引起PPAR通路的激活。     

FRRC Highlight: This note Highlights a Seminal Paper Published in Free Rad. Res. Comms. 1, 163–172 (1986): The Development of a Sensitive Analysis for 8-Hydroxy-2′-Deoxyguanosine

The development of osteonecrosis after exposure to altered air pressures is consistent with cellular injury brought about by active oxygen species. The syndrome is considered to arise as a result of an unusual combination of circumstances in which hyperoxia itself, together with the additive responses of the endocrine system to hyperoxia, hypothermia and exertion, each appear to play a part; the net result is thought to increase the mitochondrial generation of superoxide. It is suggested that effective prophylaxis may be possible primarily by establishing a nutritional status that is adequate to ensure that the functional activities of radical-scavenging systems are not hampered by deficiencies either of essential trace elements or of vitamin E. Pharmacological pretreatments designed both to decrease excessive levels of superoxide through increased catalysis of anionic dismutation and to attenuate enzyme-dependent peroxidation may provide an additional line of defence.     

Adverse effects of hyperbaric oxygen on [3H]uridine incorporation and uridine kinase activity in B104 rat neuroblastoma cells

The effects of hyperbaric oxygen on uracil nucleotide metabolism in B104 rat neuroblastoma cells were investigated. Cells exposed to 10 atm O₂ for 4 h incorporated markedly less [³H]uridine into the acid-soluble fraction and RNA compared to cells kept in ambient air. The acid-soluble fraction of the oxygen-treated cells contained less total [³H]uridine phosphates ([³H]UMP + [³H]UDP + [³H]UTP) than air-treated cells. Uridine kinase activity, assayed in cytosolic extracts from cells exposed to 10 atm O₂ for 4 h, was decreased by 46% compared to the air controls. The reduced enzyme activity which appears to account for the depressed [³H]uridine incorporation, may contribute to the lethal effects of oxygen in these cells.Abbreviations DMEM Dulbecco's Modified Eagle's Medium - Hepes 4-(2-hydroxyethyl)-1-piperazineethanesulphonic acid     

高压氧对脑缺血再灌注海马神经元Bcl-2和Bax蛋白表达的影响

目的：进一步探讨高压氧治疗脑缺血再灌注损伤,减轻神经元调亡朋而发挥保护作用的机理。方法：采用“双侧颈总动脉阻断法”前脑缺血模型,对沙土鼠前脑缺血２０ｍｉｎ后再灌注３ｄ,并用０．１５ＭＰａ和０．２５ＭＰａ压力的高压氧治疗（６０ｍｉｎ／ｄ,连续３ｄ）后,应用免疫组化ＬＳＡＢ方法,观察高压氧对海巴ＣＡ１,区神经元凋亡相关基因ｂｃｌ－２和ｂａｘ的蛋白表达的影响。结果：沙土鼠脑缺血再灌注３ｄ组海马ＣＡ１区大     

早期高压氧联合去骨瓣减压治疗重型颅脑损伤的疗效及对患者神经功能、炎性因子的影响

摘要 目的：分析早期高压氧联合去骨瓣减压治疗重型颅脑损伤的疗效及对患者神经功能、炎性因子的影响。方法：选择我院自2018年1月至2021年10月接诊的106例重型颅脑损伤患者,随机分为对照组和观察组,各53例。两组均予以常规对症支持治疗,在此基础上,对照组采取去骨瓣减压治疗,观察组采取早期高压氧联合去骨瓣减压治疗。随访3个月,比较两组治疗前后的脑代谢指标、Fugl-Meyer运动功能评分、神经功能指标、炎性因子、严重并发症发生率及近期疗效。结果：观察组治疗后脑氧摄取率（CEO₂）、混合静脉血氧饱和度（SVO₂）均高于对照组（P＜0.05）;观察组治疗后上肢、下肢及总体Fugl-Meyer运动功能评分均高于对照组（P＜0.05）;观察组治疗后血清脑源性神经营养因子（BDNF）、神经元特异性烯醇化酶（NSE）、S100β蛋白、胶质纤维酸性蛋白（GFAP）水平均低于对照组,神经生长因子（NGF）水平高于对照组（P＜0.05）;观察组治疗后血清C反应蛋白（CRP）、白介素-1β（IL-1β）、肿瘤坏死因子-α（TNF-α）均低于对照组（P＜0.05）;观察组严重并发症发生率低于对照组,预后良好率高于对照组（P＜0.05）。结论：早期高压氧联合去骨瓣减压治疗重型颅脑损伤的疗效显著,能够有效优化患者神经功能,抑制炎症反应,促进肢体运动功能恢复,进而改善预后,值得临床予以重视。