Next Article in Journal
14 MeV Neutrons for 99Mo/99mTc Production: Experiments, Simulations and Perspectives
Previous Article in Journal
Ultrasensitive (Co)polymers Based on Poly(methacrylamide) Structure with Fining-Tunable pH Responsive Value
Previous Article in Special Issue
Therapeutic Potentials of Microalgae in the Treatment of Alzheimer’s Disease
Article Menu
Issue 8 (August) cover image

Export Article

Open AccessArticle
Molecules 2018, 23(8), 1871; https://doi.org/10.3390/molecules23081871

Neuroprotective Effects of Mitochondria-Targeted Plastoquinone in a Rat Model of Neonatal Hypoxic–Ischemic Brain Injury

1
A. N. Belozersky Institute of Physico-Chemical Biology, Lomonosov Moscow State University, 119991 Moscow, Russia
2
Institute of Molecular Medicine, Sechenov First Moscow State Medical University, 119991 Moscow, Russia
3
Faculty of Fundamental Medicine, Lomonosov Moscow State University, Lomonosovsky Prospekt, house 31-5, 117192 Moscow, Russia
4
Faculty of Physics, Lomonosov Moscow State University, Leninskye gory, house 1, building 2, 119991 Moscow, Russia
*
Author to whom correspondence should be addressed.
Received: 18 June 2018 / Revised: 13 July 2018 / Accepted: 25 July 2018 / Published: 27 July 2018
Full-Text   |   PDF [1650 KB, uploaded 27 July 2018]   |  

Abstract

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 sections of the brain, SkQR1 has been shown to reduce the development of oxidative stress. Thus, the mitochondrial-targeted antioxidant derived from plant plastoquinone can effectively protect the brain of newborns both in pre-ischemic and post-stroke conditions, making it a promising candidate for further clinical studies. View Full-Text
Keywords: hypoxia–ischemia; mitochondria; mitochondria-targeted antioxidants; plastoquinone; oxidative stress hypoxia–ischemia; mitochondria; mitochondria-targeted antioxidants; plastoquinone; oxidative stress
Figures

Graphical abstract

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).
SciFeed

Share & Cite This Article

MDPI and ACS Style

Silachev, D.N.; Plotnikov, E.Y.; Pevzner, I.B.; Zorova, L.D.; Balakireva, A.V.; Gulyaev, M.V.; Pirogov, Y.A.; Skulachev, V.P.; Zorov, D.B. Neuroprotective Effects of Mitochondria-Targeted Plastoquinone in a Rat Model of Neonatal Hypoxic–Ischemic Brain Injury. Molecules 2018, 23, 1871.

Show more citation formats Show less citations formats

Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Related Articles

Article Metrics

Article Access Statistics

1

Comments

[Return to top]
Molecules EISSN 1420-3049 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top