Neuroprotective effects of mitochondria-targeted plastoquinone in a rat model of neonatal hypoxic–ischemic brain injury
Silachev D. N., Plotnikov E. Yu., Pevzner I. B., Zorova L. D., Balakireva A. V., Gulyaev M. V., Pirogov Y. A., Skulachev V. P., Zorov D. B.
Molecules
Vol.23, Issue8, Num.1871
Опубликовано: 2018
Тип ресурса: Статья
DOI:10.3390/molecules23081871
Аннотация:
Neonatal hypoxia–ischemia is one of the main causes of mortality and disability of newborns. To study the mechanisms of neonatal brain cell damage, we used a model of neonatal hypoxia–ischemia in seven-day-old rats, by annealing of the common carotid artery with subsequent hypoxia of 8[%] oxygen. We demonstrate that neonatal hypoxia–ischemia causes mitochondrial dysfunction associated with high production of reactive oxygen species, which leads to oxidative stress. Targeted delivery of antioxidants to the mitochondria can be an effective therapeutic approach to treat the deleterious effects of brain hypoxia–ischemia. We explored the neuroprotective properties of the mitochondria-targeted antioxidant SkQR1, which is the conjugate of a plant plastoquinone and a penetrating cation, rhodamine 19. Being introduced before or immediately after hypoxia–ischemia, SkQR1 affords neuroprotection as judged by the diminished brain damage and recovery of long-term neurological functions. Using vital se
Ключевые слова:
Hypoxia–ischemia; Mitochondria; Mitochondria-targeted antioxidants; Oxidative stress; Plastoquinone
10-(6'-plastoquinonyl) decylrhodamine 19; neuroprotective agent; plastoquinone; reactive oxygen metabolite; rhodamine; analogs and derivatives; animal; convalescence; disease model; drug effect; hypoxic ischemic encephalopathy; male; metabolism; mitochondrion; newborn; oxidative stress; physiology; rat; Animals; Animals, Newborn; Disease Models, Animal; Hypoxia-Ischemia, Brain; Male; Mitochondria; Neuroprotective Agents; Oxidative Stress; Plastoquinone; Rats; Reactive Oxygen Species; Recovery of Function; Rhodamines
Язык текста: Английский
ISSN: 1420-3049
Silachev D. N.
Plotnikov E. Yu. Egor Yuryevich 1980-
Pevzner I. B.
Zorova L. D.
Balakireva A. V. Anastasiya Vasilyevna 1991-
Gulyaev M. V.
Pirogov Y. A.
Skulachev V. P.
Zorov D. B.
Силачев Д. Н.
Плотников Е. Ю. Егор Юрьевич 1980-
Певзнер И. Б.
Зорова Л. Д.
Балакирева А. В. Анастасия Васильевна 1991-
Гуляев М. В.
Пирогов Y. А.
Скулачев В. П.
Зоров Д. Б.
Neuroprotective effects of mitochondria-targeted plastoquinone in a rat model of neonatal hypoxic–ischemic brain injury
Текст визуальный непосредственный
Molecules
Springer-Verlag GmbH
Vol.23, Issue8 Num.1871
2018
Статья
Hypoxia–ischemia Mitochondria Mitochondria-targeted antioxidants Oxidative stress Plastoquinone
10-(6'-plastoquinonyl) decylrhodamine 19 neuroprotective agent plastoquinone reactive oxygen metabolite rhodamine analogs and derivatives animal convalescence disease model drug effect hypoxic ischemic encephalopathy male metabolism mitochondrion newborn oxidative stress physiology rat Animals Animals, Newborn Disease Models, Animal Hypoxia-Ischemia, Brain Male Mitochondria Neuroprotective Agents Oxidative Stress Plastoquinone Rats Reactive Oxygen Species Recovery of Function Rhodamines
Neonatal hypoxia–ischemia is one of the main causes of mortality and disability of newborns. To study the mechanisms of neonatal brain cell damage, we used a model of neonatal hypoxia–ischemia in seven-day-old rats, by annealing of the common carotid artery with subsequent hypoxia of 8[%] oxygen. We demonstrate that neonatal hypoxia–ischemia causes mitochondrial dysfunction associated with high production of reactive oxygen species, which leads to oxidative stress. Targeted delivery of antioxidants to the mitochondria can be an effective therapeutic approach to treat the deleterious effects of brain hypoxia–ischemia. We explored the neuroprotective properties of the mitochondria-targeted antioxidant SkQR1, which is the conjugate of a plant plastoquinone and a penetrating cation, rhodamine 19. Being introduced before or immediately after hypoxia–ischemia, SkQR1 affords neuroprotection as judged by the diminished brain damage and recovery of long-term neurological functions. Using vital se