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Supplemental N-3 Polyunsaturated Fatty Acids Limit A1-Specific Astrocyte Polarization via Attenuating Mitochondrial Dysfunction in Ischemic Stroke in Mice.

Abstract
Ischemic stroke is one of the leading causes of death and disability for adults, which lacks effective treatments. Dietary intake of n-3 polyunsaturated fatty acids (n-3 PUFAs) exerts beneficial effects on ischemic stroke by attenuating neuron death and inflammation induced by microglial activation. However, the impact and mechanism of n-3 PUFAs on astrocyte function during stroke have not yet been well investigated. Our current study found that dietary n-3 PUFAs decreased the infarction volume and improved the neurofunction in the mice model of transient middle cerebral artery occlusion (tMCAO). Notably, n-3 PUFAs reduced the stroke-induced A1 astrocyte polarization both in vivo and in vitro. We have demonstrated that exogenous n-3 PUFAs attenuated mitochondrial oxidative stress and increased the mitophagy of astrocytes in the condition of hypoxia. Furthermore, we provided evidence that treatment with the mitochondrial-derived antioxidant, mito-TEMPO, abrogated the n-3 PUFA-mediated regulation of A1 astrocyte polarization upon hypoxia treatment. Together, this study highlighted that n-3 PUFAs prevent mitochondrial dysfunction, thereby limiting A1-specific astrocyte polarization and subsequently improving the neurological outcomes of mice with ischemic stroke.
AuthorsJun Cao, Lijun Dong, Jialiang Luo, Fanning Zeng, Zexuan Hong, Yunzhi Liu, YiBo Zhao, Zhengyuan Xia, Daming Zuo, Li Xu, Tao Tao
JournalOxidative medicine and cellular longevity (Oxid Med Cell Longev) Vol. 2021 Pg. 5524705 ( 2021) ISSN: 1942-0994 [Electronic] United States
PMID34211624 (Publication Type: Journal Article)
CopyrightCopyright © 2021 Jun Cao et al.
Chemical References
  • Fatty Acids, Omega-3
Topics
  • Animals
  • Astrocytes (metabolism)
  • Dietary Supplements (analysis)
  • Disease Models, Animal
  • Fatty Acids, Omega-3 (pharmacology, therapeutic use)
  • Ischemic Stroke (drug therapy)
  • Male
  • Mice
  • Mitochondria (drug effects)

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