A Nitric Oxide–Releasing Topical Medication as a Potential Treatment Option for Atopic Dermatitis through Antimicrobial and Anti-Inflammatory Activity

Populus deltoides, 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 P. deltoides 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 P. deltoides leaf extract might be driven by iNOS and NO inhibition mediated by modulation of the NF-κB and p38/JNK signaling pathways.

Download Full-text

Nitric Oxide Regulates Immune Cell Bioenergetic: A Mechanism to Understand Immunomodulatory Functions of Nitric Oxide-Releasing Anti-Inflammatory Drugs

The Journal of Immunology ◽

10.4049/jimmunol.173.2.874 ◽

2004 ◽

Vol 173 (2) ◽

pp. 874-882 ◽

Cited By ~ 22

Author(s):

Stefano Fiorucci ◽

Andrea Mencarelli ◽

Eleonora Distrutti ◽

Monia Baldoni ◽

Piero del Soldato ◽

...

Keyword(s):

Nitric Oxide ◽

Immune Cell ◽

Inflammatory Drugs ◽

Anti Inflammatory ◽

Nitric Oxide Releasing

Download Full-text

Ethanol Extract of Lilium Bulbs Plays an Anti-Inflammatory Role by Targeting the IKKα/β-Mediated NF-κB Pathway in Macrophages

The American Journal of Chinese Medicine ◽

10.1142/s0192415x18500672 ◽

2018 ◽

Vol 46 (06) ◽

pp. 1281-1296 ◽

Cited By ~ 9

Author(s):

Sang Yun Han ◽

Young-Su Yi ◽

Seong-Gu Jeong ◽

Yo Han Hong ◽

Kang Jun Choi ◽

...

Keyword(s):

Nitric Oxide ◽

Signaling Pathway ◽

Nuclear Translocation ◽

Inflammatory Responses ◽

Inflammatory Activity ◽

Raw264.7 Cells ◽

No Production ◽

Dependent Manner ◽

Bioactive Components ◽

Anti Inflammatory

Lilium bulbs have long been used as Chinese traditional medicines to alleviate the symptoms of various human inflammatory diseases. However, mechanisms of Lilium bulb-mediated anti-inflammatory activity and the bioactive components in Lilium bulbs remain unknown. In the present study, the anti-inflammatory activity of Lilium bulbs and the underlying mechanism of action were investigated in macrophages using Lilium bulb ethanol extracts (Lb-EE). In a dose-dependent manner, Lb-EE inhibited nitric oxide (NO) production in lipopolysaccharide (LPS)-stimulated RAW264.7 cells and bone marrow-derived macrophages (BMDMs) without causing significant cytotoxicity. Lb-EE also down-regulated mRNA expression of inflammatory genes in LPS-stimulated RAW264.7 cells, which included inducuble nitric oxide synthase (iNOS), cyclooxygenase-2 (COX2), and tumor necrosis factor-[Formula: see text] (TNF-[Formula: see text]). Furthermore, Lb-EE markedly restored LPS-induced morphological changes in RAW264.7 cells to a normal morphology. HPLC analysis identified quercetin, luteolin, and kaempferol as bioactive components contained in Lb-EE. Mechanistic studies in LPS-stimulated RAW264.7 cells revealed that Lb-EE suppressed MyD88- and TRIF-induced NF-[Formula: see text]B transcriptional activation and the nuclear translocation of NF-[Formula: see text]B transcription factors. Moreover, Lb-EE inhibited IKK[Formula: see text]/[Formula: see text]-induced activation of the NF-[Formula: see text]B signaling pathway and IKK inhibition significantly reduced NO production in LPS-stimulated RAW264.7 cells. Taken together, these results suggest that Lb-EE plays an anti-inflammatory role by targeting IKK[Formula: see text]/[Formula: see text]-mediated activation of the NF-[Formula: see text]B signaling pathway during macrophage-mediated inflammatory responses.

Download Full-text

Higenamine inhibits IL-1β-induced inflammation in human nucleus pulposus cells

Bioscience Reports ◽

10.1042/bsr20190857 ◽

2019 ◽

Vol 39 (6) ◽

Cited By ~ 2

Author(s):

Xiaoliang Bai ◽

Wenyuan Ding ◽

Sidong Yang ◽

Xiaohui Guo

Keyword(s):

Nitric Oxide ◽

Signaling Pathway ◽

Nucleus Pulposus ◽

Inflammatory Activity ◽

Nucleus Pulposus Cells ◽

Necrosis Factor Alpha ◽

Natural Progression ◽

Anti Inflammatory ◽

Inflammatory Molecules ◽

Oxide Synthase

Abstract Intervertebral disc degeneration (IDD) is a natural progression of the aging process associated with inflammation. Higenamine, a plant-based alkaloid, has been identified to possess various pharmacological properties, including anti-inflammatory activity. In the present study, we aimed to evaluate the role of higenamine in interleukin (IL)-1β-induced inflammation in human nucleus pulposus cells (NPCs). The results showed that higenamine improved cell viability in IL-1β-induced NPCs. The IL-1β-dependent up-regulation of inflammatory molecules including inducible nitric oxide synthase (iNOS), nitric oxide (NO), prostaglandin E2 (PGE2), cyclooxygenase-2 (COX-2), tumor necrosis factor alpha (TNF-α), and IL-6 was attenuated by higenamine in NPCs. The increased productions of matrix metalloproteinases (MMP-3 and MMP-13), as well as a disintegrin and metalloprotease with thrombospondin motifs (ADAMTS-4 and ADAMTS-5) were significantly mitigated by higenamine treatment. Furthermore, we also found that higenamine suppressed the IL-1β-induced activation of NF-κB signaling pathway in NPCs. In conclusion, the present study proved that higenamine exhibited anti-inflammatory activity against IL-1β-induced inflammation in NPCs via inhibiting NF-κB signaling pathway. These results suggested that higenamine might be a therapeutic agent for the treatment of IDD.

Download Full-text