Sagai Masaru, Bocci Velio
Department of Physiology, Viale A, Moro 2, 53100, University of Siena, Italy.
Med Gas Res. 2011 Dec 20;1:29. doi: 10.1186/2045-9912-1-29.
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.
本文综述了臭氧疗法的潜在作用机制。臭氧疗法的治疗效果可能部分归因于臭氧与多种生物成分反应产生的可控且适度的氧化应激。臭氧有效性与毒性之间的界限可能取决于氧化应激的强度。正如运动一样,众所周知适度运动有益健康,而过度运动则不然。严重的氧化应激会激活核转录因子κB(NFκB),通过产生COX2、PGE2和细胞因子导致炎症反应和组织损伤。然而,适度的氧化应激会激活另一种核转录因子,即核因子红细胞2相关因子2(Nrf2)。Nrf2随后诱导抗氧化反应元件(ARE)的转录。ARE的转录导致产生多种抗氧化酶,如超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(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)、药物代谢的Ⅱ相酶和热休克蛋白(HSP)。游离抗氧化剂和抗氧化酶不仅能保护细胞免受氧化和炎症的侵害,而且它们或许能够逆转慢性氧化应激。基于这些观察结果,臭氧疗法也可能通过适度的氧化应激激活Nrf2,并抑制NFκB和炎症反应。此外,Nrf2的激活可预防神经退行性疾病,如阿尔茨海默病和帕金森病。轻度免疫反应是通过其他核转录因子诱导产生的,如活化T细胞核因子(NFAT)和活化蛋白 - 1(AP - 1)。此外,臭氧疗法在血管疾病中的有效性也可以通过另一种核转录因子缺氧诱导因子 - 1α(HIF - 1α)的激活来解释,HIF - 1α也是通过适度的氧化应激诱导产生的。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皮肤病变、椎间盘突出和儿童原发性根龋病变方面的多功能性。有必要进行进一步的研究,以阐明臭氧疗法的作用机制是否涉及核转录因子,如Nrf2、NFAT、AP - 1和HIF - 1α。