无毒臭氧对h2o2诱导的应激和炎症的有益作用。

Altug Kuçukgul, S. Erdogan, Ramazan Gonenci, Gonca Ozan
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引用次数: 12

摘要

本实验研究了臭氧氧化预处理(OOP)对过氧化氢(H2O2)诱导的人肺泡细胞的抗氧化和抗炎作用。在MTT和台盼蓝活力试验中,100 μmol/L的H2O2分别使活细胞数量减少17.3%和21.9%,而20 μmol/L的臭氧使细胞增殖再生,分别防止了9.6%和11.0%的细胞损失。H2O2使过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GPx)和超氧化物歧化酶(SOD)的转录水平分别降低5.43-、2.89-和5.33倍,使Bax、NF-κβ、TNF-α和iNOS的表达分别升高1.57-、1.32-、1.40-和1.41倍。然而,臭氧预处理使CAT、GPx和SOD的转录水平分别提高7.08倍、5.17倍和6.49倍,使Bax、NF-κβ、TNF-α和iNOS的转录水平分别降低1.25倍、0.76倍、3.63倍和7.91倍。H2O2处理组细胞内谷胱甘肽(GSH)水平和SOD活性分别降低46.2%和45.0%,OOP恢复了H2O2引起的58.5%和20.1%的损伤。H2O2也使亚硝酸盐含量增加了7.84倍,而OOP将这一增加减少了一半。结果表明,OOP对体外氧化应激性肺损伤模型具有较强的抗氧化和抗炎作用。
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Beneficial effects of nontoxic ozone on H2O2-induced stress and inflammation.
In this study, the anti-oxidant and anti-inflammatory efficacy of ozone oxidative preconditioning (OOP) were investigated on hydrogen peroxide (H2O2)-induced human lung alveolar cells. In MTT and trypan blue viability tests, while 100 μmol/L H2O2 caused a 17.3% and 21.9% decrease in the number of living cells, respectively, ozone at 20 μmol/L regenerated cell proliferation and prevented 9.6% and 11.0% of cell loss, respectively. In addition, H2O2 decreased the transcription levels of catalase (CAT), glutathione peroxidase (GPx), and superoxide dismutase (SOD) 5.43-, 2.89-, and 5.33-fold, respectively, while it increased Bax, NF-κβ, TNF-α, and iNOS expression 1.57-, 1.32-, 1.40-, and 1.41-fold, respectively. Ozone pretreatment, however, increased CAT, GPx, and SOD transcription levels 7.08-, 5.17-, and 6.49-fold and decreased Bax, NF-κβ, TNF-α, and iNOS transcriptions by 1.25-, 0.76-, 3.63-, and 7.91-fold, respectively. Moreover, intracellular glutathione (GSH) level and SOD activity were decreased by 46.2% and 45.0% in the H2O2 treatment group, and OOP recovered 58.5% and 20.1% of the decreases caused by H2O2. H2O2 also increased nitrite levels 7.84-fold, and OOP reduced this increase by half. Consequently, OOP demonstrated potent anti-oxidant and anti-inflammatory effects on in vitro model of oxidative stress-induced lung injury.
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