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Beneficial effects of nontoxic ozone on H2O2-induced stress and inflammation
被引:17
|作者:
Kucukgul, Altug
[1
]
Erdogan, Suat
[2
]
Gonenci, Ramazan
[3
]
Ozan, Gonca
[4
]
机构:
[1] Mustafa Kemal Univ, Fac Vet, Dept Biochem, TR-31060 Antakya, Turkey
[2] Trakya Univ, Dept Med Biol, Fac Med, TR-22050 Edirne, Turkey
[3] Mustafa Kemal Univ, Fac Vet, Dept Surg, TR-31060 Antakya, Turkey
[4] Firat Univ, Fac Vet, Dept Biochem, TR-23200 Elazig, Turkey
关键词:
oxidative stress;
inflammation;
ozone oxidative preconditioning;
lung alveolar cells;
OXIDATIVE STRESS;
REACTIVE OXYGEN;
CANCER;
DAMAGE;
CELLS;
ISCHEMIA/REPERFUSION;
APOPTOSIS;
INJURY;
D O I:
10.1139/bcb-2016-0033
中图分类号:
Q5 [生物化学];
Q7 [分子生物学];
学科分类号:
071010 ;
081704 ;
摘要:
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 mu mol/L H2O2 caused a 17.3% and 21.9% decrease in the number of living cells, respectively, ozone at 20 mu mol/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-kappa beta, TNF-alpha, 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-kappa beta, TNF-alpha, 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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页码:577 / 583
页数:7
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