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1.
Chinese Journal of Hepatobiliary Surgery ; (12): 191-195, 2017.
Article in Chinese | WPRIM | ID: wpr-514320

ABSTRACT

Objective To explore the protective effect of ozone oxidative preconditioning on hepatic ischemia reperfusion injury in rats.Methods Eighteen 8-week-old SPF Sprague-Dawley male rats weighting 250 ~300 g were randomly divided into three groups (n =6 each):sham operation group (group S),ischemia/reperfusion group (group I/R) and ozone oxidative preconditioning group (group O3 + I/R).In Group O3 + I/R,rats received five-day preconditioning treatments by intraperitoneal injection of ozone and oxygen mixed gases (ozone concentration 50 mg/L,1 mg · kg-1 · d-1),and then experienced the procedure of hepatic ischemia/reperfusion injury.Model of hepatic ischemia/reperfusion injury was established by clamping the branches of hepatic artery and portal vein in the median and left lateral hepatic lobes for 45 min,followed by 3-h reperfusion.After reperfusion,blood samples were taken from the aorta abdominalis for detecting serum aminotransferases (ALT & AST).These rats were executed and the hepatic tissue samples were collected for measuring hepatic malondialdehyde (MDA) and superoxide dismutase (SOD) level.Results Compared with group S,concentrations of serum ALT,AST and hepatic MDA were increased in group I/R and O3 + I/R;concentrations of hepatic SOD were decreased (P < 0.05) in group I/R,but concentration of hepatic SOD was increased in group O3 + I/R.Compared with group IR,concentrations of serum ALT,AST and hepatic MDA were decreased,while concentration of hepatic SOD was increased in group O3 + I/R (P < 0.05).Conclusion Ozone oxidative preconditioning could inhibit the lipid peroxidation to protect the rats against hepatic ischemia/reperfusion injury.

2.
Braz. j. med. biol. res ; 46(9): 789-796, 19/set. 2013. tab, graf
Article in English | LILACS | ID: lil-686574

ABSTRACT

Ionizing radiation causes its biological effects mainly through oxidative damage induced by reactive oxygen species. Previous studies showed that ozone oxidative preconditioning attenuated pathophysiological events mediated by reactive oxygen species. As inhalation of ozone induces lung injury, the aim of this study was to examine whether ozone oxidative preconditioning potentiates or attenuates the effects of irradiation on the lung. Rats were subjected to total body irradiation, with or without treatment with ozone oxidative preconditioning (0.72 mg/kg). Serum proinflammatory cytokine levels, oxidative damage markers, and histopathological analysis were compared at 6 and 72 h after total body irradiation. Irradiation significantly increased lung malondialdehyde levels as an end-product of lipoperoxidation. Irradiation also significantly decreased lung superoxide dismutase activity, which is an indicator of the generation of oxidative stress and an early protective response to oxidative damage. Ozone oxidative preconditioning plus irradiation significantly decreased malondialdehyde levels and increased the activity of superoxide dismutase, which might indicate protection of the lung from radiation-induced lung injury. Serum tumor necrosis factor alpha and interleukin-1 beta levels, which increased significantly following total body irradiation, were decreased with ozone oxidative preconditioning. Moreover, ozone oxidative preconditioning was able to ameliorate radiation-induced lung injury assessed by histopathological evaluation. In conclusion, ozone oxidative preconditioning, repeated low-dose intraperitoneal administration of ozone, did not exacerbate radiation-induced lung injury, and, on the contrary, it provided protection against radiation-induced lung damage.


Subject(s)
Animals , Female , Lung Injury/prevention & control , Lung/radiation effects , Oxidative Stress/physiology , Ozone/therapeutic use , Radiation Injuries, Experimental/prevention & control , Chromatography, High Pressure Liquid , Enzyme-Linked Immunosorbent Assay , Interleukin-1beta/blood , Malondialdehyde/blood , Rats, Wistar , Radiation-Protective Agents/therapeutic use , Superoxide Dismutase/metabolism , Tumor Necrosis Factor-alpha/blood
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