• The Korea Journal of Herbology
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• v.21 no.3
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• pp.103-109
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• 2006

Objectives : The purpose of this study was to investigate the TLR-4 mediated anti-inflammatory effects of extract from Xanthii Fructus(XF) on the peritoneal macrophage. Methods : To evaluate of TLR-4 mediated inflammatory of XF, we examined NO and cytokine production in TRL-4 ligand(LPS-lipopolysacchride) induced macrophages. Furthermore, we checked molecular mechanism using western blot. Results : l.Extract from XF reduced LPS-induced Nitric oxide (NO), tumor necrosis factor-a (TNF-a), interleukin (IL)-6 and IL-12 production in peritoneal macrophages 2.Extract from XF itself does not have any cytotoxic effect.XS inhibited degradation of IkBa in the TLR-4 mediated peritoneal macrophages Conclusion : XF down-regulated TLR4 ligand(LPS)-induced NO and cytokine productions.

• Journal of Microbiology and Biotechnology
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• v.18 no.7
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• pp.1308-1316
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• 2008

Propionibacterium acnes is known to playa pivotal role in the pathogenesis of acne vulgaris. CBT-SL5 is one of the antimicrobial peptides from Enterococcus faecalis SL5, and it has shown antimicrobial activity against P. acnes. The aim of this study was to investigate the anti-inflammatory effect of CBT-SL5 on the inflammation induced by P. acnes in cultured human keratinocyes. Cultured human keratinocytes derived from neonatal foreskin were treated with heat-killed P. acnes to induce inflammation, and then various concentrations of CBT-SL5 were added to the P. acnes-treated keratinocytes. The mRNA expression and protein secretion of interleukin (IL)-8, an inflammation marker, was analyzed by real-time reverse transcription polymerase chain reaction and enzyme-linked immunosorbent assay, respectively. We also analyzed the nuclear factor-kappa B (NF-$\kappaB$) p65 translocation by performing immunofluorescent staining. P. acnes treatment up regulated the IL-8 mRNA expression in the keratinocytes, and this was brought about through both toll-like receptor (TLR)2 and TLR4. At the concentrations of 10, 50, and 100 ng/ml, CBT-SL5 significantly down regulated the P. acnes-induced IL-8 mRNA expression and protein production (p<0.05). At 6 hand 12 h of the treatment, CBT-SL5 significantly suppressed the P. acnes-induced IL-8 mRNA expression. Secretion of IL-8 protein was significantly reduced at 24 h. The functional inhibitory activity of CBT-SL5 was shown by CBT-SL5 suppressing the P. acnes-induced NF-$\kappaB$ translocation from the cytoplasm to the nucleus. These results demonstrated that CBT-SL5 suppressed the P. acnes-induced IL-8 expression in keratinocytes. Therefore, CBT-SL5 may be a novel anti-inflammatory treatment for acne.

• Korean Journal of Plant Resources
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• v.35 no.5
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• pp.565-573
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• 2022

Gingival inflammation is one of the main causes that can be related to various periodontal diseases. Human gingival fibroblast (HGF) is the major constituent in periodontal connective tissue and secretes various inflammatory mediators, such as nitric oxide (NO) and prostaglandin E₂ (PGE₂), upon lipopolysaccharide stimulation. This study is aimed at investigating the anti-inflammatory and antioxidative activities of Lotus Root extract (LRE) in Porphyromonas gingivalis derived lipopolysaccharide (LPS-PG)-stimulated HGF-1 cells. The concentration of NO and PGE₂, as well as their responsible enzymes, inducible NO synthase (iNOS), and cyclooxygenase-2 (COX-2), was analyzed by Griess reaction, ELISA, and western blot analysis. LPS-PG sharply elevated the production and protein expression of inflammatory mediators, which were significantly attenuated by LRE treatment in a dose-dependent manner. LRE treatment also suppressed activation of Toll-like receptor 4 (TLR4)/myeloid differentiation primary response gene 88 (MyD88) and nuclear factor-κB (NF-κB) in LPS-PG-stimulated HGF-1 cells. In addition, one of phase II enzyme, NAD(P)H quinone dehydrogenase (NQO)-1, and its transcription factor, Nuclear factor erythroid 2-related factor 2 (Nrf2), were significantly induced by LRE treatment. Consequently, these results suggest that LRE ameliorates LPS-PG-induced inflammatory responses by attenuating TLR4/MyD88-mediated NF-κB, and activating NQO-1/Nrf2 antioxidant response element signaling pathways in HGF-1 cells.

• Korean Journal of Plant Resources
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• v.36 no.1
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• pp.15-25
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• 2023

Myriophyllum spicatum L. has been used as an ornamental in ponds and aquariums, and as a folk remedy for inflammation and pus. Nevertheless, the biological activity and underlying mechanisms of anti-inflammatory effects are unclear. This study is aimed at investigating the antioxidative and anti-inflammatory activities of ethanol extract of Myriophyllum spicatum L. (EMS) in lipopolysaccharide (LPS)-stimulated RAW 264.7 cells. Antioxidant activity of EMS was assessed by radical-scavenging effects on ferric reducing antioxidant power (FRAP) and 2,2-diphenyl-1-picrylhydrazyl (DPPH) free radicals. As inflammatory response parameters produced by LPS-stimulated RAW 264.7 cells were quantified to assess the anti-inflammatory activity of EMS. Our results showed that EMS increased FRAP and DPPH radical-scavenging activity. In EMS-treated RAW 264.7 cells, the production of NO, PGE₂, TNF-α and IL-1β was significantly inhibited at the non-cytotoxic concentration. In addition, EMS significantly attenuated LPS-stimulated the toll-like receptor (TLR) 4/myeloid differentiation protein (MyD) 88 signaling pathway, and inhibited nuclear translocation of nuclear factor-kappa B(NF-κB). Positive correlations were noted between anti-inflammatory activity and antioxidant activity. In conclusion, it was indicated that EMS suppresses the transcription of inflammatory factors by inhibiting the TLR4/MyD88/NF-κB signaling pathway, thereby suppressing LPS-stimulated inflammation in RAW 264.7 cells. This study highlights the potential role of EMS against inflammation and associated diseases.

• Journal of Life Science
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• v.25 no.9
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• pp.993-999
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• 2015

The beetle Popillia flavosellata has been no reported its functional effects. In this study, we investigated the anti-inflammatory effect of P. flavosellata ethanol extract (PFE) on RAW 264.7 mouse macrophage cells treated with lipopolysaccharide (LPS) for the induction of inflammation. First, we examined the cytotoxicity of PFE in the RAW 264.7 cells at a concentration of 2,000 μg/ml or less. To evaluate the anti-inflammatory effects of PFE, we investigated the expression levels of proinflammatory cytokines, such as tumor necrosis factor (TNF)-α and interleukin (IL)-6, and proinflammatory enzymes, such as inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in LPS-induced RAW 264.7 cells. In addition, we examined whether PFE inhibited the translocation of nuclear factor kappa B (NF-κB) p65 into the nucleus in the LPS-induced RAW 264.7 cells. We found that the protein levels of TNF-α and IL-6 were decreased in the LPS-induced RAW 264.7 cells after the treatment with PFE in a dose-dependent manner. In addition, we confirmed that PFE inhibited the translocation of NF-κB p65 into the nucleus, as well as the protein expression levels of iNOS and COX-2. Accordingly, we propose that PFE exerts an anti-inflammatory effect through the down-regulation of NF-κB p65, TNF-α, IL-6, iNOS, and COX-2 via the toll like receptor (TLR)-4 inflammatory signaling pathway.

• Journal of Life Science
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• v.34 no.7
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• pp.443-452
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• 2024

This study aimed to examine the influence of 3,6-anhydroxygalactose (L-AHG) on the pro-inflammatory M1 polarization and pro-inflammatory responses observed in the RAW264.7 mouse macrophage cell line following stimulation with lipopolysaccharides (LPS). L-AHG exhibited a significant and dose-dependent inhibition of inducible nitric oxide synthase (iNOS) expression, a hallmark of M1 polarization, and subsequent NO production in LPS-stimulated RAW264.7 cells. Furthermore, the LPS-induced upregulation of cyclooxygenase-2 (COX-2), which drives the production of prostaglandin E2, an inflammatory mediator, was also inhibited by L-AHG. L-AHG did not affect the LPS-triggered Toll-like receptor 4 (TLR4)-mediated pro-inflammatory signaling pathway, which culminated in the activation of transforming growth factor-β-activated kinase 1 (TAK1). However, it was observed to inhibit the generation of reactive oxugen species (ROS) in a dose-dependent manner, as well as the TAK1-driven activation of JNK and p38 MAPK. Given that the active p38 MAPK is known to contribute to the assembly of active nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, which catalyzes the intracellular generation of pro-inflammatory ROS in LPS-stimulated macrophages, the dose-dependent reduction in the LPS-induced ROS generation by L-AHG may be mainly due to the prevention of TAK1-driven activation of p38 MAPK. Together, these results demonstrate that the L-AHG-mediated inhibition of the TAK1-JNK/p38 MAPK activation phase of the pro-inflammatory signaling pathway in LPS-stimulated RAW264.7 cells by L-AHG represents a promising mechanism for suppressing M1 polarization and pro-inflammatory responses in macrophages.