4.6 Article

Long-term dietary supplementation with plant-derived omega-3 fatty acid improves outcome in experimental ischemic stroke

期刊

ATHEROSCLEROSIS
卷 325, 期 -, 页码 89-98

出版社

ELSEVIER IRELAND LTD
DOI: 10.1016/j.atherosclerosis.2021.04.005

关键词

Inflammation; alpha-linolenic acid; Omega-3 fatty acid; Ischemic stroke; Dietary intervention

资金

  1. Swiss National Science Foundation (SNSF) [310030_197510, 310030_144152]
  2. Alfred and Annemarie von Sick Grants for Translational and Clinical Research Cardiology and Oncology
  3. Swiss Heart Foundation
  4. Foundation for Cardiovascular Research-Zurich Heart House
  5. Kardio Foundation
  6. Sheikh Khalifa's Foundation Assistant Professorship at the Faculty of Medicine, University of Zurich
  7. SNSFPRIMA [PR00P3_179861/1]
  8. Swiss National Science Foundation (SNF) [310030_144152, 310030_197510, PR00P3_179861] Funding Source: Swiss National Science Foundation (SNF)

向作者/读者索取更多资源

A long-term dietary intervention with ALA has been shown to reduce stroke size and neurological dysfunction, maintain BBB integrity, and decrease inflammation. These findings suggest that ALA supplementation could pave the way for novel stroke treatments.
Background and aims: Early revascularization -the gold standard therapy for ischemic stroke- is often withheld in the elderly population due to high risk of complications. Thus, safe and effective preventive and therapeutic options are needed. The plant-derived omega-3-fatty-acid alpha-linolenic-acid (ALA) has emerged as a novel cardiovascular-protective agent. As of yet, little is known about its potential therapeutic effects on stroke. We hereby aimed to investigate the impact of a clinically relevant long-term dietary intervention with ALA on stroke outcome. Methods: Six month-old C57BL/6 wildtype males were either fed an ALA-rich (high ALA) or a control diet (low ALA) for 12 months. At 18 months, brain ischemia/reperfusion was induced by transient middle cerebral artery occlusion (tMCAO). Stroke size and neurological function were assessed. Functional blood-brain-barrier-(BBB) permeability and protein expression were assessed by immunohistochemistry. Baseline inflammatory markers were measured at 18 months. Results: High ALA-fed animals displayed decreased circulating TNF-alpha levels and Neutrophil-to-Lymphocyte Ratios at 18 months. Stroke size and neurological dysfunction were significantly reduced in high ALA-fed animals. Coherently to the reduced stroke size, functional BBB integrity and occludin endothelial expression were maintained by high ALA supplementation. Additionally, ALA reduced endothelial activation and thus recruitment and activation of macrophages and resident microglia. Finally, high ALA diet reduced the expression of BBB-degrading and neurotoxic MMP-3 and MMP-9. Conclusions: We demonstrate the beneficial effects of a clinically relevant and feasible dietary intervention with a safe and readily available compound in the setting of stroke. The protective effects observed with ALA supplementation may relate to blunting of inflammation and might pave the way for novel stroke treatments.

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