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Fisetin Suppresses Pulmonary Inflammatory Responses Through Heme Oxygenase-1 Mediated Downregulation of Inducible Nitric Oxide Synthase

Journal of Medicinal Food 2020년 23권 11호 p.1163 ~ 1168
심현채, 추삼열, 김재홍, 백문창, 배종섭,
소속 상세정보
심현채 ( Sim Hyun-Chae ) - Kyungpook National University College of Pharmacy
추삼열 ( Choo Sam-Yeol ) - Kyungpook National University College of Pharmacy
김재홍 ( Kim Jae-Hong ) - Gachon University College of Medicine Department of Biochemistry
백문창 ( Baek Moon-Chang ) - Kyungpook National University Department of Molecular Medicine
배종섭 ( Bae Jong-Sup ) - Kyungpook National University College of Pharmacy

Abstract


The effects of a mixture of fisetin on cytokine-mediated pulmonary damages have not been studied, despite its known antiviral, neuroprotective, and anti-inflammatory activities. Using lipopolysaccharide (LPS)-activated human pulmonary artery endothelial cells (HPAECs), we determined the effects of fisetin on the induction of heme oxygenase-1 (HO-1), inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2). In the lung tissue of LPS-treated mice, fisetin was also evaluated for its effect on the regulation of iNOS and tumor necrosis factor (TNF)-α. In LPS-activated HPAECs, fisetin increased nuclear factor erythrocyte 2-related factor 2-antioxidant response element (Nrf2-ARE) reporter activity through the nuclear translocation of Nrf2, and the expression of HO-1, and decreased IL-1β and iNOS/NO production. In particular, the suppression of iNOS/NO expression by the administration of fisetin was dependent on HO-1. Current findings indicate that the anti-inflammatory activity of fisetin was due to its HO-1 dependent downregulation of p-STAT-1 and nuclear factor kappa B (NF-κB) and the resultant inhibition of iNOS, and also suggest TNF-α as a potential target for HO-1. We propose that administration of fisetin may be a novel approach, ideal for the treatment of inflammatory pulmonary disease.

키워드

fisetin; HO-1; iNOS; p-STAT-1

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