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Mechanisms of Action Involved in Ozone Therapy: Is healing induced via a mild oxidative stress?

机译：臭氧治疗的作用机理：是否通过轻度的氧化应激诱导愈合？

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The potential mechanisms of action of ozone therapy are reviewed in this paper. The therapeutic efficacy of ozone therapy may be partly due the controlled and moderate oxidative stress produced by the reactions of ozone with several biological components. The line between effectiveness and toxicity of ozone may be dependent on the strength of the oxidative stress. As with exercise, it is well known that moderate exercise is good for health, whereas excessive exercise is not. Severe oxidative stress activates nuclear transcriptional factor kappa B (NFκB), resulting in an inflammatory response and tissue injury via the production of COX2, PGE2, and cytokines. However, moderate oxidative stress activates another nuclear transcriptional factor, nuclear factor-erythroid 2-related factor 2 (Nrf2). Nrf2 then induces the transcription of antioxidant response elements (ARE). Transcription of ARE results in the production of numerous antioxidant enzymes, such as SOD, GPx, glutathione-s-transferase(GSTr), catalase (CAT), heme-oxygenase-1 (HO-1), NADPH-quinone-oxidoreductase (NQO-1), phase II enzymes of drug metabolism and heat shock proteins (HSP). Both free antioxidants and anti-oxidative enzymes not only protect cells from oxidation and inflammation but they may be able to reverse the chronic oxidative stress. Based on these observations, ozone therapy may also activate Nrf2 via moderate oxidative stress, and suppress NFκB and inflammatory responses. Furthermore, activation of Nrf2 results in protection against neurodegenerative diseases, such as Alzheimer's and Parkinson's diseases. Mild immune responses are induced via other nuclear transcriptional factors, such as nuclear factor of activated T-cells (NFAT) and activated protein-1 (AP-1). Additionally, the effectiveness of ozone therapy in vascular diseases may also be explained by the activation of another nuclear transcriptional factor, hypoxia inducible factor-1α (HIF-1a), which is also induced via moderate oxidative stress. Recently these concepts have become widely accepted. The versatility of ozone in treating vascular and degenerative diseases as well as skin lesions, hernial disc and primary root carious lesions in children is emphasized. Further researches able to elucidate whether the mechanisms of action of ozone therapy involve nuclear transcription factors, such as Nrf2, NFAT, AP-1, and HIF-1α are warranted.
机译：本文综述了臭氧治疗的潜在作用机理。臭氧疗法的治疗功效可能部分归因于臭氧与几种生物成分的反应所产生的受控和适度的氧化应激。臭氧的有效性和毒性之间的界线可能取决于氧化应激的强度。与运动一样，众所周知，适度运动有益于健康，而过度运动则不利。严重的氧化应激会激活核转录因子κB（NFκB），通过产生COX2，PGE2和细胞因子而导致炎症反应和组织损伤。但是，适度的氧化应激会激活另一个核转录因子，即核因子-类胡萝卜素2相关因子2（Nrf2）。然后，Nrf2诱导抗氧化剂反应元件（ARE）的转录。 ARE的转录导致产生多种抗氧化酶，例如SOD，GPx，谷胱甘肽S-转移酶（GSTr），过氧化氢酶（CAT），血红素加氧酶-1（HO-1），NADPH醌氧化还原酶（NQO）。 -1），药物代谢和热休克蛋白（HSP）的II期酶。游离的抗氧化剂和抗氧化酶不仅可以保护细胞免于氧化和炎症，而且还能够逆转慢性氧化应激。基于这些观察结果，臭氧疗法还可通过适度的氧化应激激活Nrf2，并抑制NFκB和炎症反应。此外，Nrf2的激活导致针对神经退行性疾病（例如阿尔茨海默氏病和帕金森氏病）的保护。轻度免疫反应是通过其他核转录因子诱导的，例如活化T细胞（NFAT）和活化蛋白1（AP-1）的核因子。此外，臭氧疗法在血管疾病中的有效性也可以通过激活另一种核转录因子，即低氧诱导因子-1α（HIF-1a）来解释，该因子也可通过中等氧化应激诱导。最近，这些概念已被广泛接受。强调了臭氧在治疗血管和退行性疾病以及儿童皮肤病变，椎间盘突出症和原发性龋齿病变中的多功能性。有必要进行进一步的研究以阐明臭氧治疗的作用机制是否涉及核转录因子，例如Nrf2，NFAT，AP-1和HIF-1α。

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