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Ellagic Acid Prevents Particulate Matter-Induced Pulmonary Inflammation and Hyperactivity in Mice: A Pilot Study

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  • Sunyoung Jeong

    (Bioanalytical and Pharmacokinetic Research Group, Korea Institute of Toxicology, Daejeon 34114, Republic of Korea
    Department of Human and Environmental Toxicology, University of Science and Technology, Daejeon 34113, Republic of Korea
    These authors contributed equally to this work.)

  • Sungryong Bae

    (Department of Fire Protection and Disaster Management, Chosun University, Gwangju 61452, Republic of Korea
    These authors contributed equally to this work.)

  • Eui-Cheol Shin

    (Department of GreenBio Science/Food Science and Technology, Gyeongsang National University, Jinju 52725, Republic of Korea
    These authors contributed equally to this work.)

  • Jong-Hwa Lee

    (Bioanalytical and Pharmacokinetic Research Group, Korea Institute of Toxicology, Daejeon 34114, Republic of Korea
    Department of Human and Environmental Toxicology, University of Science and Technology, Daejeon 34113, Republic of Korea)

  • Jung-Heun Ha

    (Department of Food Science and Nutrition, Dankook University, Cheonan 31116, Republic of Korea
    Research Center for Industrialization of Natural Neutralization, Dankook University, Yongin 16890, Republic of Korea)

Abstract

The inhalation of fine particulate matter (PM) is a significant health-related environmental issue. Previously, we demonstrated that repeated PM exposure causes hyperlocomotive activity in mice, as well as inflammatory and hypoxic responses in their lungs. In this study, we evaluated the potential efficacy of ellagic acid (EA), a natural polyphenolic compound, against PM-induced pulmonary and behavioral abnormalities in mice. Four treatment groups were assigned in this study ( n = 8): control (CON), particulate-matter-instilled (PMI), low-dose EA with PMI (EL + PMI), and high-dose EA with PMI (EH + PMI). EA (20 and 100 mg/kg body weight for low dose and high dose, respectively) was orally administered for 14 days in C57BL/6 mice, and after the eighth day, PM (5 mg/kg) was intratracheally instilled for 7 consecutive days. PM exposure induced inflammatory cell infiltration in the lungs following EA pretreatment. Moreover, PM exposure induced inflammatory protein expression in the bronchoalveolar lavage fluid and the expression of inflammatory (tumor necrosis factor alpha ( Tnfα ), interleukin ( Il ) -1b , and Il-6 ) and hypoxic (vascular endothelial growth factor alpha ( Vegfα ), ankyrin repeat domain 37 ( Ankrd37 )) response genes. However, EA pretreatment markedly prevented the induction of expression of inflammatory and hypoxic response genes in the lungs. Furthermore, PM exposure significantly triggered hyperactivity by increasing the total moving distance with an increase in moving speed in the open field test. On the contrary, EA pretreatment significantly prevented PM-induced hyperactivity. In conclusion, dietary intervention with EA may be a potential strategy to prevent PM-induced pathology and activity.

Suggested Citation

  • Sunyoung Jeong & Sungryong Bae & Eui-Cheol Shin & Jong-Hwa Lee & Jung-Heun Ha, 2023. "Ellagic Acid Prevents Particulate Matter-Induced Pulmonary Inflammation and Hyperactivity in Mice: A Pilot Study," IJERPH, MDPI, vol. 20(5), pages 1-16, March.
    • Handle: RePEc:gam:jijerp:v:20:y:2023:i:5:p:4523-:d:1086966
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    References listed on IDEAS

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    1. Hueng-Chuen Fan & Chuan-Mu Chen & Jeng-Dau Tsai & Kuo-Liang Chiang & Stella Chin-Shaw Tsai & Ching-Ying Huang & Cheng-Li Lin & Chung Y. Hsu & Kuang-Hsi Chang, 2022. "Association between Exposure to Particulate Matter Air Pollution during Early Childhood and Risk of Attention-Deficit/Hyperactivity Disorder in Taiwan," IJERPH, MDPI, vol. 19(23), pages 1-10, December.
    2. Sunyoung Jeong & Jong-Hwa Lee & Jung-Heun Ha & Jinhee Kim & Inyong Kim & Sungryong Bae, 2021. "An Exploratory Study of the Relationships Between Diesel Engine Exhaust Particle Inhalation, Pulmonary Inflammation and Anxious Behavior," IJERPH, MDPI, vol. 18(3), pages 1-13, January.
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