Cheng Heyun, Lu Rui, Du Juan, Zhao Xingjuan, Zhuang Zhijiang
Department of Neurology, The Fifth Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Front Med (Lausanne). 2025 Jul 25;12:1595568. doi: 10.3389/fmed.2025.1595568. eCollection 2025.
Ozonated autohemotherapy is a therapeutic method that utilizes the contact of medical ozone with blood to achieve the effect of ozone oxidative preconditioning, and then re-infuses it back into the human body. It has the functions of alleviating oxidative stress damage, reducing neuroexcitation toxicity, and mitigating cellular edema and inflammatory responses. Cerebral infarction has a significant social hazard, and there are multiple treatment methods available. There have been reports of treating cerebral infarction with ozonated autohemotherapy, but the efficacy and mechanism of action are not yet clear. The background now includes information about the proteins measured, specifically neuron-specific enolase (NSE) and S100β protein, which are markers of neuronal cell damage.
A randomized controlled study was conducted, enrolling 62 patients with acute cerebral infarction to investigate the therapeutic effect of ozonated autohemotherapy on acute cerebral infarction. The study included three groups: a control group, an oxygen placebo group, and an ozone therapy group. The intervention was administered over a period of 5 days, with patients undergoing treatment within 24 h of symptom onset. Inclusion criteria comprised patients diagnosed with acute cerebral infarction, aged >18 years, with an NIHSS score between 4 and 15. Exclusion criteria included other neurological disorders, severe infectious diseases, and contraindications for ozone therapy. The efficacy was primarily evaluated through neurological function scoring, motor function scoring, cognitive scoring, and the detection of neuron-specific enolase (NSE) and S100β protein (A neurotrophic factor), which are markers of neuronal cell damage. The two genes involved in the study are HIF-1 and Nrf-2. The mechanism of ozonated autohemotherapy in treating acute cerebral infarction was also explored by detecting these two genes and three indicators related to oxidative stress in the body.
Ozonated autohemotherapy significantly improved the prognosis of acute cerebral infarction, with NIHSS scores decreasing by 30%, Barthel Index scores increasing by 25%, and MoCA scores improving by 20% compared to the control group. Levels of NSE and S100- protein were reduced by 25 and 30%, respectively, compared to baseline. In the ozone treatment group, superoxide dismutase (SOD) and malondial Dehyde (MDA) levels decreased, while glutathione peroxidase (GSH-Px) levels increased, and both HIF-1 and Nrf-2 levels were elevated compared to before. Moreover, it did not increase the risk of heart, liver, and kidney damage.
It suggests that ozone may improve oxidative stress by regulating HIF-1 and Nrf-2, reduce the oxidative stress response and inflammatory damage caused by ischemia of neuronal cells in acute cerebral infarction, thereby improving neurological function and prognosis. The treatment method is safe in the short term. Long-term safety requires further research.
臭氧自血疗法是一种利用医用臭氧与血液接触以达到臭氧氧化预处理效果，然后再回输到人体的治疗方法。它具有减轻氧化应激损伤、降低神经兴奋毒性以及减轻细胞水肿和炎症反应的功能。脑梗死具有重大的社会危害性，且有多种治疗方法。已有用臭氧自血疗法治疗脑梗死的报道，但疗效及作用机制尚不清楚。目前的背景信息包括所检测的蛋白质，具体为神经元特异性烯醇化酶（NSE）和S100β蛋白，它们是神经元细胞损伤的标志物。
进行了一项随机对照研究，纳入62例急性脑梗死患者，以研究臭氧自血疗法对急性脑梗死的治疗效果。该研究包括三组：对照组、氧气安慰剂组和臭氧治疗组。干预为期5天，患者在症状发作后24小时内接受治疗。纳入标准包括诊断为急性脑梗死、年龄>18岁、美国国立卫生研究院卒中量表（NIHSS）评分在4至15分之间的患者。排除标准包括其他神经系统疾病、严重传染病以及臭氧治疗的禁忌证。疗效主要通过神经功能评分、运动功能评分、认知评分以及检测神经元特异性烯醇化酶（NSE）和S100β蛋白（一种神经营养因子，为神经元细胞损伤的标志物）来评估。研究涉及的两个基因是缺氧诱导因子-1（HIF-1）和核因子E2相关因子2（Nrf-2）。还通过检测这两个基因以及体内与氧化应激相关的三个指标来探讨臭氧自血疗法治疗急性脑梗死的机制。
与对照组相比，臭氧自血疗法显著改善了急性脑梗死的预后，NIHSS评分降低了30%，Barthel指数评分提高了25%，蒙特利尔认知评估量表（MoCA）评分提高了20%。与基线相比，NSE和S100β蛋白水平分别降低了25%和30%。在臭氧治疗组中，超氧化物歧化酶（SOD）和丙二醛（MDA）水平降低，而谷胱甘肽过氧化物酶（GSH-Px）水平升高，且HIF-1和Nrf-2水平均较之前升高。此外，它并未增加心、肝、肾损伤的风险。
这表明臭氧可能通过调节HIF-1和Nrf-2来改善氧化应激，减轻急性脑梗死中神经元细胞缺血引起的氧化应激反应和炎症损伤，从而改善神经功能和预后。该治疗方法在短期内是安全的。长期安全性需要进一步研究。
