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高压氧疗法改善肢体缺血后的新生血管形成——减轻活性氧的作用

Hyperbaric Oxygen Therapy Improved Neovascularisation Following Limb Ischaemia-The Role of ROS Mitigation.

作者信息

Lin You-Cheng, Shih Jhih-Yuan, Lin Yu-Wen, Niu Ko-Chi, Hong Chon-Seng, Chen Zhih-Cherng, Pan Shin-Chen, Chang Tzu-Yen, Kan Wei-Chih, Chang Wei-Ting

机构信息

Division of Plastic Surgery, Department of Surgery, Chi-Mei Medical Center, Tainan, Taiwan.

Division of Cardiology, Department of Internal Medicine, Chi Mei Medical Center, Tainan, Taiwan.

出版信息

J Cell Mol Med. 2024 Dec;28(24):e70310. doi: 10.1111/jcmm.70310.

DOI:10.1111/jcmm.70310
PMID:39720917
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11669187/
Abstract

Hyperbaric oxygen (HBO) therapy has emerged as a potential treatment, shown to enhance blood flow and angiogenesis. However, specific effects and mechanisms of HBO on limb ischaemia responding to a hypoxic environment remain largely unknown. We aimed to investigate the therapeutic potential of HBO in the treatment of limb ischaemia. Following limb ischaemia surgery, we evaluated the angiogenic capacity in wild-type C57BL/6J mice subjected to HBO treatment (100% oxygen at 3 ATA for 1 h/day for five consecutive days) compared to untreated controls. Notably, through laser Doppler perfusion imaging and CD31 staining mice receiving HBO postlimb ischaemia surgery exhibited significantly enhanced angiogenic capability and reduced ROS expression compared to nontreated counterparts. Additionally, in vitro experiments were conducted to investigate whether HBO could mitigate endothelial cell dysfunction and reactive oxygen species (ROS) production triggered by oxygen-glucose deprivation (OGD). HBO treatment rescued the impaired proliferation, migration and tube formation of endothelial cells following OGD. Mechanistically, HBO upregulated the expression of proangiogenic proteins, including vascular endothelial growth factor (VEGF), haem oxygenase-1 (HO-1), hypoxia-inducible factor 1 (HIF-1) and nuclear factor erythroid 2-related factor 2 (Nrf2). Collectively, HBO treatment shows promise in augmenting the endogenous angiogenic potential and suppressing ROS levels in limb ischaemia.

摘要

高压氧(HBO)疗法已成为一种潜在的治疗方法,已证明其可促进血流和血管生成。然而,HBO对肢体缺血应对缺氧环境的具体作用和机制仍 largely未知。我们旨在研究HBO在治疗肢体缺血方面的治疗潜力。在肢体缺血手术后,我们评估了接受HBO治疗(在3个绝对大气压下吸入100%氧气,每天1小时,连续5天)的野生型C57BL/6J小鼠与未治疗的对照组相比的血管生成能力。值得注意的是,通过激光多普勒灌注成像和CD31染色,与未治疗的小鼠相比,肢体缺血手术后接受HBO治疗的小鼠表现出显著增强的血管生成能力和降低的ROS表达。此外,进行了体外实验,以研究HBO是否可以减轻氧糖剥夺(OGD)引发的内皮细胞功能障碍和活性氧(ROS)产生。HBO治疗挽救了OGD后内皮细胞受损的增殖、迁移和管腔形成。从机制上讲,HBO上调了促血管生成蛋白的表达,包括血管内皮生长因子(VEGF)、血红素加氧酶-1(HO-1)、缺氧诱导因子1(HIF-1)和核因子红细胞2相关因子2(Nrf2)。总体而言,HBO治疗在增强肢体缺血的内源性血管生成潜力和抑制ROS水平方面显示出前景。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/941d/11669187/04f671a37bb0/JCMM-28-e70310-g006.jpg
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本文引用的文献

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