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Effect of Xenon Treatment on Gene Expression in Brain Tissue after Traumatic Brain Injury in Ratsстатья
Информация о цитировании статьи получена из
Web of Science
Статья опубликована в журнале из списка Web of Science и/или Scopus
Дата последнего поиска статьи во внешних источниках: 8 декабря 2021 г.
- Авторы: Filev Anton D., Silachev Denis N., Ryzhkov Ivan A., Lapin Konstantin N., Babkina Anastasiya S., Grebenchikov Oleg A., Pisarev Vladimir M.
- Журнал: BRAIN SCIENCES
- Том: 11
- Номер: 7
- Год издания: 2021
- Первая страница: 889
- Номер статьи: 7
- DOI: 10.3390/brainsci11070889
- Аннотация: The overactivation of inflammatory pathways and/or a deficiency of neuroplasticity may result in the delayed recovery of neural function in traumatic brain injury (TBI). A promising approach to protecting the brain tissue in TBI is xenon (Xe) treatment. However, xenon’s mechanisms of action remain poorly clarified. In this study, the early-onset expression of 91 target genes was investigated in the damaged and in the contralateral brain areas (sensorimotor cortex region) 6 and 24 h after injury in a TBI rat model. The expression of genes involved in inflammation, oxidation, antioxidation, neurogenesis and neuroplasticity, apoptosis, DNA repair, autophagy, and mitophagy was assessed. The animals inhaled a gas mixture containing xenon and oxygen (ϕXe = 70%; ϕO2 25–30% 60 min) 15–30 min after TBI. The data showed that, in the contralateral area, xenon treatment induced the expression of stress genes (Irf1, Hmox1, S100A8, and S100A9). In the damaged area, a trend towards lower expression of the inflammatory gene Irf1 was observed. Thus, our results suggest that xenon exerts a mild stressor effect in healthy brain tissue and has a tendency to decrease the inflammation following damage, which might contribute to reducing the damage and activating the early compensatory processes in the brain post-TBI.
- Добавил в систему: Писарев Владимир Митрофанович