Anti-Inflammatory Activity of Populus deltoides Leaf Extract via Modulating NF-κB and p38/JNK Pathways

• Published in: International journal of molecular sciences Vol. 19; no. 12; p. 3746
• Main Authors: Jeong, Ye Eun, Lee, Mi-Young
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 25.11.2018; MDPI
• Subjects: anti-inflammation; Anti-inflammatory agents; c-Jun protein; Cyclooxygenase-2; Cytokines; Extracellular signal-regulated kinase; Gene expression; Herbal medicine; Inflammation; Inflammatory diseases; iNOS; Investigations; Kinases; Leaves; Lipopolysaccharides; MAP kinase; MAPK; NF-κB; NF-κB protein; Nitric oxide; Nitric-oxide synthase; Nuclear transport; Phosphorylation; Plant extracts; Populus deltoides; Populus deltoides leaf; Prostaglandin E2; Protein kinase; Proteins; Signal transduction; Terminal protein; Transcription factors; Tumor necrosis factor-TNF; Tumor necrosis factor-α; Populus deltoides leaf; NF-κB; iNOS; anti-inflammation; MAPK
• ISSN: 1422-0067; 1661-6596; 1422-0067
• DOI: 10.3390/ijms19123746

, known as eastern cottonwood, has been commonly used as a medicinal plant. The aim of the present study was to investigate the mechanism underlying the anti-inflammatory activity of leaf extract (PLE). PLE effectively inhibited the expression of inducible nitric oxide synthase (iNOS) and nitric oxide (NO) production in lipopolysaccharide (LPS)-stimulated RAW 264.7 cells, but not that of cyclooxygenase-2 (COX-2) and prostaglandin E2. Proinflammatory tumor necrosis factor alpha (TNF-α) levels were also reduced by the extract. PLE inhibited the phosphorylation of nuclear factor-kappa B (NF-κB) and inhibitor of Kappa Bα (IκBα), and blunted LPS-triggered enhanced nuclear translocation of NF-κB p65. In mitogen-activated protein kinase (MAPK) signaling, PLE effectively decreased the phosphorylation of p38 and c-Jun N-terminal protein kinase (JNK), but not of extracellular signal-regulated kinase 1/2 (ERK1/2). Taken together, these results suggest that anti-inflammatory activity of leaf extract might be driven by iNOS and NO inhibition mediated by modulation of the NF-κB and p38/JNK signaling pathways.