ArticleOncotarget2018
PM2.5 inhalation induces intracranial atherosclerosis which may be ameliorated by omega 3 fatty acids.
Article in Oncotarget, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
14 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.
- Outdoor Air Pollution and Brain Structure and Function From Across Childhood to Young Adulthood: A Methodological Review of Brain MRI Studies.Frontiers in public health · 2019Pooled it
- Long-term exposure to PMScientific reports · 2025Article
- AMPK agonist AICAR ameliorates maternal hepatic lipid metabolism disorder, inflammation, and fibrosis caused by PMScientific reports · 2025Article
- Pollution characteristics and health risk assessment of heavy metals in PM2.5 in Fuxin, China.Environmental geochemistry and health · 2024Article
- Alterations in the Blood Kynurenine Pathway Following Long-Term PM2.5 and PM10 Exposure: A Cross-Sectional Study.Biomedicines · 2024Article
- Intersection of Aging and Particulate Matter 2.5 Exposure in Real World: Effects on Inflammation and Endocrine Axis Activities in Rats.International journal of endocrinology · 2024Article
- Modern Concepts of the Role of Fine Particles (PM 2.5) in the Genesis of Atherosclerosis and Myocardial Damage: Clinical and Epidemiological Data, the Main Pathophysiological Mechanisms.Current cardiology reviews · 2023Review
- Adverse effects of air pollution-derived fine particulate matter on cardiovascular homeostasis and disease.Trends in cardiovascular medicine · 2022Review
- The Role of Fine Particles (PM 2.5) in the Genesis of Atherosclerosis and Myocardial Damage: Emphasis on Clinical and Epidemiological Data, and Pathophysiological Mechanisms.Cardiology research · 2022Review
- A review of respirable fine particulate matter (PMFrontiers in molecular neuroscience · 2022Review
- Phosphoenolpyruvate Carboxykinase (PCK) in the Brain Gluconeogenic Pathway Contributes to Oxidative and Lactic Injury After Stroke.Molecular neurobiology · 2021Article
- Filtered air intervention reduces inflammation and hypothalamus-pituitary-adrenal axis activation in adult male and female rats after PM 2.5 exposure.Environmental science and pollution research international · 2020Article
- Amelioration of PMRespiratory research · 2019Article
- Particulate air pollution: major research methods and applications in animal models.Environmental diseaseArticle
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundIntracranial atherosclerosis (ICA) a major health problem. This study investigated whether inhalation of fine airborne particulate matters (PM2.5) causes ICA and whether omega-3 fatty acids (O3FA) attenuated the development of ICA.
resultsTwelve but not 6 week exposure significantly increased triglycerides (TG) in normal chow diet (NCD), while PM2.5 enhanced all lipid profiles (TG, low density lipoprotein (LDL) and cholesterol (CHO)) after both 6 and 12-week exposure with high-cholesterol diet (HCD). PM2.5 exposure for 12 but not 6 weeks significantly induced middle cerebral artery (MCA) narrowing and thickening, in association with the enhanced expression of inflammatory cytokines, (interleukin 6 (IL-6), tumor necrosis factor alpha (TNF-α), monocyte chemoattractant protein-1 (MCP-1), interferon gamma (IFN-γ)), vascular cell adhesion molecule 1 (VCAM-1) and inducible nitric oxide synthase (iNOS). O3FA significantly attenuated vascular alterations, even without favorable changes in lipid profiles, in association with reduced expression of IL-6, TNF-α, MCP-1, IFN-γ, VCAM-1 and iNOS in brain vessels.
conclusionsPM2.5 exposure for 12 weeks aggravates ICA in a dietary model (HCD + short-term L-NAME), which may be mediated by vascular inflammation. O3FA dietary supplementation prevents ICA development and inflammatory reaction in cerebral vessels.
methodsAdult Sprague-Dawly rats were under filtered air (FA) or PM2.5 exposure with NCD or HCD for 6 or 12 weeks. Half of the HCD rats were treated with O3FA (5 mg/kg/day) by gavage. A total of 600 mg NG-nitro-L-arginine methyl ester (L-NAME, 3 mg/mL) per rat was administered over two weeks as supplementation in the HCD group. Blood lipids, including LDL, CHO, TG and high density lipoprotein (HDL), were measured at 6 and 12 weeks. ICA was determined by lumen diameter and thickness of the MCA. Inflammatory markers, IL-6, TNF-α, MCP-1, IFN-γ, VCAM-1 and iNOS were assessed by real-time PCR for mRNA and Western blot for protein expression.
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