Methyl p‑hydroxycinnamate exerts anti‑inflammatory effects in mouse models of lipopolysaccharide‑induced ARDS
Autor: | Seong-Man Kim, Jung Hee Kim, Seung Ho Kim, Jin-Mi Park, Soo Hyeon Goo, Jae-Hong Min, Jae-Won Lee, Jae Hoon Oh, Juhyun Lee, Wanjoo Chun, Jinseon Choi, Sukmo Kang, Kyung-Seop Ahn |
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Rok vydání: | 2021 |
Předmět: |
Lipopolysaccharides
Male Cancer Research Lipopolysaccharide medicine.drug_class Anti-Inflammatory Agents methyl p-hydroxycinnamate Pharmacology Biochemistry Anti-inflammatory NF-κB chemistry.chemical_compound Mice Downregulation and upregulation inflammatory cell Genetics medicine Macrophage Animals Molecular Biology Inflammation Respiratory Distress Syndrome biology Monocyte heme oxygenase-1 Articles acute respiratory distress syndrome Nitric oxide synthase Mice Inbred C57BL Disease Models Animal medicine.anatomical_structure RAW 264.7 Cells Oncology chemistry Gene Expression Regulation Apoptosis Cinnamates biology.protein Molecular Medicine Tumor necrosis factor alpha Signal Transduction |
Zdroj: | Molecular Medicine Reports |
ISSN: | 1791-3004 |
Popis: | Methyl p-hydroxycinnamate (MH), an esterified derivative of p-Coumaric acid exerts anti-inflammatory effects on lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages. Based on these effects, the present study investigated the protective role of MH in a mouse model of LPS-induced acute respiratory distress syndrome (ARDS). The results demonstrated that administration of LPS (5 mg/kg intranasally) markedly increased the neutrophil/macrophage numbers and levels of inflammatory molecules (TNF-α, IL-6, IL-1β and reactive oxygen species) in the bronchoalveolar lavage fluid (BALF) of mice. On histological examination, the presence of inflammatory cells was observed in the lungs of mice administered LPS. LPS also notably upregulated the secretion of monocyte chemoattractant protein-1 and protein content in BALF as well as expression of inducible nitric oxide synthase in the lungs of mice; it also caused activation of p38 mitogen-activated protein kinase (MAPK) and NF-κB signaling. However, MH treatment significantly suppressed LPS-induced upregulation of inflammatory cell recruitment, inflammatory molecule levels and p38MAPK/NF-κB activation, and also led to upregulation of heme oxygenase-1 (HO-1) expression in the lungs of mice. In addition, the ability of MH to induce HO-1 expression was confirmed in RAW264.7 macrophages. Taken together, the findings of the present study indicated that MH may exert protective effects against airway inflammation in ARDS mice by inhibiting inflammatory cell recruitment and the production of inflammatory molecules. |
Databáze: | OpenAIRE |
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