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高压氧疗法可减轻烧伤所致失神经肌肉萎缩。

Hyperbaric Oxygen Therapy Attenuates Burn-Induced Denervated Muscle Atrophy.

机构信息

Department of Anesthesiology, Kaohsiung Municipal Ta-Tung Hospital, Kaohsiung, Taiwan.

Department of Anesthesiology, Kaohsiung Medical University Hospital, Kaohsiung, Kaohsiung Medical University, Taiwan.

出版信息

Int J Med Sci. 2021 Oct 25;18(16):3821-3830. doi: 10.7150/ijms.65976. eCollection 2021.

DOI:10.7150/ijms.65976
PMID:34790058
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8579280/
Abstract

Neuronal apoptosis and inflammation in the ventral horn of the spinal cord contribute to denervated muscle atrophy post-burn. Hyperbaric oxygen therapy (HBOT) exerts anti-inflammation and neuroprotection. Furthermore, hypoxia-inducible factor (HIF)-1α has been reported to promote inflammation and apoptosis. We investigated the therapeutic potential of HBOT and the role of HIF-1α post-burn. Sprague-Dawley rats were divided into three groups: a control group, an untreated burn group receiving burn and sham treatment, and a HBOT group receiving burn injury and HBOT. The burn injury was induced with 75ºC ± 5ºC at the right hindpaw. HBOT (100% oxygen at 2.5 atmosphere, 90 min/day) and sham HBOT (21% oxygen at 1 atmosphere, 90 min/day) was started on day 28 after burn injury and continued for 14 treatments (days 28-41). Incapacitance (hind limb weight bearing) testing was conducted before burn and weekly after burn. At day 42 post-burn, the gastrocnemius muscle and the spinal cord ventral horn were analyzed. HBOT improved burn-induced weight bearing imbalance. At day 42 post-burn, less gastrocnemius muscle atrophy and fibrosis were noted in the HBOT group than in the untreated burn group. In the ventral horn, HBOT attenuated the neuronal apoptosis and glial activation post-burn. The increases in phosphorylated AKT/mTOR post-burn were reduced after HBOT. HBOT also inhibited HIF-1α signaling, as determined by immunofluorescence and western blot. HBOT reduces burn-induced neuronal apoptosis in the ventral horn, possibly through HIF-1α signaling.

摘要

脊髓腹角的神经元凋亡和炎症导致烧伤后失神经肌肉萎缩。高压氧治疗(HBOT)具有抗炎和神经保护作用。此外,缺氧诱导因子(HIF)-1α已被报道可促进炎症和细胞凋亡。我们研究了 HBOT 治疗烧伤后的潜力以及 HIF-1α 的作用。

SD 大鼠分为三组:对照组、未治疗烧伤组(接受烧伤和假处理)和 HBOT 组(接受烧伤和 HBOT)。使用 75°C±5°C 的温度在右后爪诱导烧伤。HBOT(2.5 个大气压的 100%氧气,每天 90 分钟)和假 HBOT(1 个大气压的 21%氧气,每天 90 分钟)于烧伤后第 28 天开始,持续治疗 14 天(第 28-41 天)。烧伤前和烧伤后每周进行一次失力量测。烧伤后第 42 天,分析比目鱼肌和脊髓腹角。

HBOT 改善了烧伤引起的负重平衡失调。烧伤后第 42 天,HBOT 组的比目鱼肌萎缩和纤维化程度低于未治疗烧伤组。在腹角,HBOT 减轻了烧伤后的神经元凋亡和神经胶质激活。HBOT 还减少了磷酸化 AKT/mTOR 的增加,这表明 HBOT 可能通过 HIF-1α 信号通路发挥作用。

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