Ozone reduces ischemic damage after a stroke by regulating the autophagy of astrocytes

Stroke is a common and damaging disease of brain tissue, and has high morbidity, disability, and mortality rates. Ozone (O₃) is an isomer of oxygen and can be applied to ozonate the isolated blood in specific containers outside the body and return it to the body. O₃ can also alter the activity and function of multiple cellular components, thus affecting blood viscosity and altering hemodynamics. However, the question of whether O₃ has clinical value in the treatment of stroke requires further investigation. This study sought to evaluate the protective effect and possible mechanism of O₃ in brain injury after stroke.

First, oxygen-glucose deprivation/reoxygenation (OGD/R)-induced human glioblastoma cell (A172) and middle cerebral artery occlusion (MCAO) rat models were established. Second, the levels of the associated ribonucleic acids and proteins were analyzed using reverse-transcription real-time-quantitative polymerase chain reaction, Western Blot, or immunofluorescence assays. Third, the concentration of glutamate and lactate dehydrogenase (LDH) were assessed using enzyme-linked immunoassays.

The results showed that glial fibrillary acidic protein was upregulated in the OGD/R A172 cells. O₃ decreased LDH and increased glutamate levels in the OGD/R A172 cells, which suggests that O₃ reduced brain damage in the in vitro stroke model. We also showed that O₃ attenuated brain infarction in the in-vivo stroke model. Further, we found that O₃ alleviated stroke-induced brain damage by reducing the apoptosis of astrocytes. Further, the B-cell lymphoma 2 inhibitor propofol alleviated stroke-induced brain damage.

Thus, O₃ notably alleviated stroke-induced brain damage by inhibiting the apoptosis of astrocytes in the OGD/R-induced human glioblastoma cell and MACO rat models.