直肠臭氧治疗对免疫球蛋白A缺乏症氧化应激的保护作用

Jacqueline Díaz Luis, S. Menéndez Cepero, M. M. Machado Cano, Lucia Fariñas Rodríguez, Maikel Roque Morgado
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摘要

自由基的过量产生导致促氧化剂和抗氧化剂之间失衡,有利于前者;这会导致氧化还原控制信号的丢失和对生物分子如蛋白质、脂质和脱氧核糖核酸的损伤。当参与免疫应答的细胞氧化还原代谢的稳态被改变时,它们通常演变成氧化应激的情况,从而促进细胞功能障碍和死亡。我们的工作目的是研究臭氧对氧化还原状态的调节作用,氧化还原状态是维持免疫球蛋白A缺乏症患者正常免疫功能所必需的。患者和方法:研究伦理委员会进行并批准了一项临床试验,其患者知情同意纳入。60例患者随机分为两组:一组接受臭氧直肠注入(研究组- sg),另一组使用Hebertrans®皮下注入(对照组- gc组)。测定促氧化参数(丙二醛- mda和高级氧化蛋白产物- aopp)和抗氧化参数(超氧化物歧化酶- sod1、过氧化氢酶- cat、谷胱甘肽过氧化物酶- gpx和血清总抗氧化能力)。分别在治疗开始时和治疗后一个月进行测量。结果:SG组15岁患者的MDA和APOP较对照组显著降低(p = 0.000)。与GC相比,15岁(p = 0.006)和16 ~ 30岁(p = 0.040)患者SG中SOD1升高。与初始值相比,15年SG患者的CAT显著增加(p=0.001)。患者SG总抗氧化能力的最终结果显著(p=0.000)高于对照组。15年后,GPx得到了类似的结果(p=0.013)。结论:臭氧治疗对氧化还原平衡有良好的影响。医疗臭氧治疗可能是一种额外的治疗选择,免疫球蛋白A缺乏患者氧化应激。
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Protective effect of rectal ozone therapy against oxidative stress in immunoglobulin A deficiency
The excess in the production of free radicals produces an imbalance between the prooxidants and antioxidants in favor of the former; which causes loss of redox control signaling and damage to biomolecules such as proteins, lipids and deoxyribonucleic acid. When homeostasis is altered in the redox metabolism of cells that participate in the immune response, they usually evolve into a situation of oxidative stress that facilitates cell dysfunction and death. The objective of our work was to study the effect of ozone on the regulation of redox status, necessary to maintain normal immune function in patients with immunoglobulin A deficiency. Patients and methods: The Research Ethics Committee conducted and approved a clinical trial and whose patients gave informed consent for inclusion. Sixty patients were randomly assigned to two groups: one receiving ozone rectal insufflation (study group-SG) and the second using Hebertrans® (control-GC group), subcutaneously. Pro-oxidant parameters (malondialdehyde-MDA and advanced oxidation protein products-AOPP) and antioxidant parameters (superoxide dismutase1-SOD1, catalase-CAT, glutathione peroxidase-GPx and total antioxidant capacity of serum) were measured. They were measured at the beginning and one month after treatment. Results: In the SG the MDA and the APOP of patients ?15 years, decreased significantly (p = 0.000) with respect to the control group. SOD1 in the SG increased in patients ?15 years (p = 0.006) and from 16 to 30 years of age (p = 0.040) with respect to GC. CAT in patients ?15 years of the SG increased significantly (p=0.001) with respect to initial values. The final result of the total antioxidant capacity in the SG was significantly (p=0.000) higher in patients ? 15 years, similar results were obtained in GPx (p=0.013). Conclusions: With ozone therapy, beneficial effects on the oxidation reduction balance were achieved. Medical ozone therapy may be an additional treatment option, for immunoglobulin A deficient patients with oxidative stress.
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