Fisetin Suppresses Pulmonary Inflammatory Responses through Heme Oxygenase-1 Mediated Downregulation of Inducible Nitric Oxide Synthase
- Authors
- Sim, Hyunchae; Choo, Samyeol; Kim, Jaehong; Baek, Moon-Chang; Bae, Jong-Sup
- Issue Date
- Nov-2020
- Publisher
- MARY ANN LIEBERT, INC
- Keywords
- fisetin; HO-1; iNOS; p-STAT-1
- Citation
- JOURNAL OF MEDICINAL FOOD, v.23, no.11, pp.1163 - 1168
- Journal Title
- JOURNAL OF MEDICINAL FOOD
- Volume
- 23
- Number
- 11
- Start Page
- 1163
- End Page
- 1168
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/79071
- DOI
- 10.1089/jmf.2020.4755
- ISSN
- 1096-620X
- 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)-alpha. 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-1 beta 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-kappa B) and the resultant inhibition of iNOS, and also suggest TNF-alpha 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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