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The let-7 microRNA enhances heme oxygenase-1 by suppressing Bach1 and attenuates oxidant injury in human hepatocytes.let-7微小RNA通过抑制Bach1增强血红素加氧酶-1并减轻人肝细胞中的氧化损伤。
Biochim Biophys Acta. 2012 Nov-Dec;1819(11-12):1113-22. doi: 10.1016/j.bbagrm.2012.06.001. Epub 2012 Jun 12.
2
Resveratrol-sensitized UVA induced apoptosis in human keratinocytes through mitochondrial oxidative stress and pore opening.白藜芦醇敏化 UVA 诱导人角质形成细胞凋亡通过线粒体氧化应激和孔开放。
J Photochem Photobiol B. 2012 Aug 1;113:42-50. doi: 10.1016/j.jphotobiol.2012.04.013. Epub 2012 May 18.
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Free radicals and extrinsic skin aging.自由基与皮肤外源性老化。
Dermatol Res Pract. 2012;2012:135206. doi: 10.1155/2012/135206. Epub 2012 Feb 29.
4
Attenuating inflammation but stimulating both angiogenesis and neurogenesis using hyperbaric oxygen in rats with traumatic brain injury.高压氧治疗创伤性脑损伤大鼠:减轻炎症,同时刺激血管生成和神经发生。
J Trauma Acute Care Surg. 2012 Mar;72(3):650-9. doi: 10.1097/TA.0b013e31823c575f.
5
Impaired vasodilation in the pathogenesis of hypertension: focus on nitric oxide, endothelial-derived hyperpolarizing factors, and prostaglandins.高血压发病机制中的血管舒张功能障碍:聚焦一氧化氮、内皮衍生超极化因子和前列腺素。
J Clin Hypertens (Greenwich). 2012 Apr;14(4):198-205. doi: 10.1111/j.1751-7176.2012.00606.x.
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Mechanisms of IFN-γ-induced apoptosis of human skin keratinocytes in patients with atopic dermatitis.IFN-γ 诱导特应性皮炎患者皮肤角质形成细胞凋亡的机制。
J Allergy Clin Immunol. 2012 May;129(5):1297-306. doi: 10.1016/j.jaci.2012.02.020. Epub 2012 Mar 24.
7
Ellagic acid protects human keratinocyte (HaCaT) cells against UVA-induced oxidative stress and apoptosis through the upregulation of the HO-1 and Nrf-2 antioxidant genes.鞣花酸通过上调 HO-1 和 Nrf-2 抗氧化基因保护人角质形成细胞(HaCaT)细胞免受 UVA 诱导的氧化应激和凋亡。
Food Chem Toxicol. 2012 May;50(5):1245-55. doi: 10.1016/j.fct.2012.02.020. Epub 2012 Feb 22.
8
A retrospective study of diabetic foot ulcers treated with hyperbaric oxygen therapy.高压氧治疗糖尿病足溃疡的回顾性研究。
Int Wound J. 2012 Dec;9(6):665-76. doi: 10.1111/j.1742-481X.2011.00936.x. Epub 2012 Feb 28.
9
Cell type-dependent gene transcription profile in a three-dimensional human skin tissue model exposed to low doses of ionizing radiation: implications for medical exposures.三维人体皮肤组织模型中细胞类型依赖性基因转录谱在低剂量电离辐射暴露下的变化:对医疗照射的意义。
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10
Acute sensitization of colon cancer cells to inflammatory cytokines by prophase arrest.有丝分裂前期阻滞使结肠癌细胞对炎症细胞因子变得敏感。
Biochem Pharmacol. 2012 May 1;83(9):1217-28. doi: 10.1016/j.bcp.2012.01.024. Epub 2012 Jan 25.

高压氧预处理可保护皮肤免受 UVA 损伤。

Hyperbaric oxygen preconditioning protects skin from UV-A damage.

机构信息

Department of Molecular and Cell Biology, University of Connecticut, 91 North Eagleville Road, U3125, Storrs, CT 06269, USA.

出版信息

Cell Stress Chaperones. 2013 Jan;18(1):97-107. doi: 10.1007/s12192-012-0362-2. Epub 2012 Aug 3.

DOI:10.1007/s12192-012-0362-2
PMID:22855227
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3508122/
Abstract

Hyperbaric oxygen therapy (HBOT) is used for a number of applications, including the treatment of diabetic foot ulcers and CO poisoning. However, we and others have shown that HBOT can mobilize cellular antioxidant defenses, suggesting that it may also be useful under circumstances in which tissue protection from oxidative damage is desired. To test the protective properties of hyperbaric oxygen (HBO) on a tissue level, we evaluated the ability of a preconditioning treatment regimen to protect cutaneous tissue from UV-A-induced oxidative damage. Three groups of hairless SKH1-E mice were exposed to UV-A 3 days per week for 22 weeks, with two of these groups receiving an HBO pretreatment either two or four times per week. UV-A exposure increased apoptosis and proliferation of the skin tissue, indicating elevated levels of epithelial damage and repair. Pretreatment with HBO significantly reduced UV-A-induced apoptosis and proliferation. A morphometric analysis of microscopic tissue folds also showed a significant increase in skin creasing following UV-A exposure, which was prevented by HBO pretreatment. Likewise, skin elasticity was found to be greatest in the group treated with HBO four times per week. The effects of HBO were also apparent systemically as reductions in caspase-3 activity and expression were observed in the liver. Our findings support a protective function of HBO pretreatment from a direct oxidative challenge of UV-A to skin tissue. Similar protection of other tissues may likewise be achievable.

摘要

高压氧疗法(HBOT)用于多种应用,包括治疗糖尿病足溃疡和一氧化碳中毒。然而,我们和其他人已经表明,HBOT 可以动员细胞抗氧化防御,这表明它在需要防止氧化损伤的情况下也可能有用。为了在组织水平上测试高压氧(HBO)的保护特性,我们评估了预处理方案保护皮肤组织免受 UV-A 诱导的氧化损伤的能力。三组无毛 SKH1-E 小鼠每周接受 UV-A 照射 3 天,其中两组每周接受两次或四次 HBO 预处理。UV-A 暴露会增加皮肤组织的细胞凋亡和增殖,表明上皮损伤和修复水平升高。HBO 预处理可显著减少 UV-A 诱导的细胞凋亡和增殖。对微观组织褶皱的形态计量分析也表明,UV-A 暴露后皮肤褶皱明显增加,而 HBO 预处理可预防这种增加。同样,每周接受 HBO 治疗四次的组的皮肤弹性最大。HBO 的作用也在系统中表现出来,因为观察到肝组织中的半胱天冬酶-3 活性和表达降低。我们的研究结果支持 HBO 预处理对皮肤组织直接氧化应激的保护作用。其他组织也可能同样获得类似的保护。