The effect of medical ozone on oxidative stress and neuroinflammation in the early stage after experimental status epilepticus

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Çokyaman T., Öztopuz R. Ö., Coşkun Ö., Buyuk B., Kiraz H. A., Elmas S.

BIOLOGIA, vol.76, no.12, pp.3875-3882, 2021 (SCI-Expanded) identifier identifier

  • Publication Type: Article / Article
  • Volume: 76 Issue: 12
  • Publication Date: 2021
  • Doi Number: 10.1007/s11756-021-00911-w
  • Journal Name: BIOLOGIA
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED)
  • Page Numbers: pp.3875-3882
  • Keywords: Status epilepticus, Ozone, Pilocarpine, Lithium, Rats, Neuroprotection, HYPERBARIC-OXYGEN, PILOCARPINE, PATHOPHYSIOLOGY, ACTIVATION, MORTALITY, ISCHEMIA, NEURONS, INJURY, RATS
  • Çanakkale Onsekiz Mart University Affiliated: Yes


Preservation of the brain is important to reducing recurrent seizures and other neurological sequelae after status epilepticus (SE). Medical ozone (MedO(3)) shows antioxidant, anti-inflammatory and anti-apoptotic properties in the human body. In this study, it was aimed to understand the neuroprotective potential of MedO(3) in the acute period after SE. Mature rats of Wistar Albino were used for the study. Group design O-3 + SE: SE induced after MedO(3), O-3: MedO(3) alone was given, SE: SE only induced, SE + O-3; MedO(3) given after SE, C: control and S: sham control group. SE was induced with lithium-pilocarpine experimental model and evaluated on the Racine scale. Peripheral blood samples and brain tissue samples were taken before decapitation. Histopathological evaluation of the hippocampus of the rats given medical O-3 before and after SE were studied. The highest peripheral blood oxidative stress index (OSI) was found in SE group. The OSI level in O-3 + SE and SE + O-3 was significantly higher than SE/C/S. Gene expressions of TNF-alpha and IL-1 beta mRNA were significantly higher in SE compared to other groups. Histopathologically; eosinophilia, cellular shrinkage and interstitial oedema were detected in the most severe SE and to a lesser extent in O-3 + SE/ SE + O-3. MedO(3) reduced SE-induced oxidative damage, neuroinflammation and neuronal injury and contributed positively to neuroprotection.