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KMID : 1161420200230111163
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Journal of Medicinal Food
2020 Volume.23 No. 11 p.1163 ~ p.1168
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Fisetin Suppresses Pulmonary Inflammatory Responses Through Heme Oxygenase-1 Mediated Downregulation of Inducible Nitric Oxide Synthase
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Sim Hyun-Chae
Choo Sam-Yeol
Kim Jae-Hong
Baek Moon-Chang
Bae Jong-Sup
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Abstract
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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.
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KEYWORD
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fisetin, HO-1, iNOS, p-STAT-1
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