• IMMUNE NETWORK
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• v.12 no.5
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• pp.213-216
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• 2012

Our previous report showed that polyacetylene compound, 1-Heptadecene-11, 13-diyne-8, 9, 10-triol (PA) from the root of Cirsium japonicum var. ussuriense has anti-inflammatory activity. In this study we investigated the role of the PA as inhibitor of caspase-1, which converts prointerleukin-$1{\beta}$ (proIL-$1{\beta}$) to active IL-$1{\beta}$ and is activated by inflammasome involved in the inflammatory process. We tested the effect of PA on the production of pro-inflammatory cytokines, IL-$1{\beta}$ in murine macrophage cell line, RAW264.7. PA inhibited lipopolysaccharide (LPS)-induced IL-$1{\beta}$ production by macrophages at a dose dependent manner. PA also suppressed the activation of caspase-1. The mRNA level of ASC (apoptosis-associated spec-like protein containing a CARD), an important adaptor protein of inflammasome, was decreased in the PA treated group. Therefore our results suggest that the anti-inflammatory effect of PA is due to inhibit the caspase-1 activation.

• Microbiology and Biotechnology Letters
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• v.48 no.3
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• pp.366-372
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• 2020

Since, side effects of antibiotics are frequently emphasized these days, their use is gradually diminishing, and alternative drugs are being developed. We have sought to reintroduce them as raw materials for human health as conventional 'weapons' that have been retired after their historical duties. In this study, we investigated the anti-inflammatory effects of lincomycin (LIN), on lipopolysaccharide (LPS)-stimulated RAW 264.7 cells. Our findings show that LIN potently inhibited production of LPS-induced proinflammatory mediators, such as nitric oxide (NO) and prostaglandin E₂ (PGE₂), without cytotoxicity. Consistent with these findings, LIN strongly decreased protein expression levels of inducible NO synthase (iNOS) and cyclooxygenase (COX-2). Furthermore, LIN reduced pro-inflammatory cytokines such as tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-1β. To further elucidate the mechanisms of these inhibitory effects of LIN, we studied LPS-induced IκB-α degradation, and mitogen-activated protein kinase (MAPK) phosphorylation. LIN suppressed downregulation of inhibitory κB (IκB-α) degradation, and the phosphorylation of the c-Jun N-terminal kinase (JNK) pathway. Based on these results, we suggest that LIN may be considered a potential candidate as an anti-inflammatory cosmetic or a medicine for human health.

• Journal of Physiology & Pathology in Korean Medicine
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• v.24 no.1
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• pp.80-84
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• 2010

Codonopsis Lanceolata (CL) has been widely used in Oriental medicine for treatment of chronic inflammatory diseases, such as bronchitis, cough, and spasm; however, the mechanism of its anti-inflammatory activity has not been clarified. In this study, therefore, we investigated the inhibitory effect of CL on LPS-induced inflammation. The effect of CL was analyzed by ELISA, RT-PCR and Western blotting in LPS-stimulated RAW264.7 cells. We found that CL suppressed not only the mRNA expression of pre-inflammatory cytokines, inducible nitric oxide synthase (iNOS), and cyclooxygenase (COX)-2, but also the phosphorylation of ERK1/2, JNK1/2 and p38 MAPK. These results suggest that CL exerts an anti-inflammatory effect through the regulation of the mitogen-activated protein kinases (MAPK) pathway, thereby decreasing production of pre-inflammatory cytokines, NO, and PGE2.

• Biomedical Science Letters
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• v.25 no.1
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• pp.92-98
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• 2019

Metformin is a drug used for the treatment of diabetes and is associated with anti-inflammatory reaction, but the underlying mechanism is unclear. In this study, we investigated the effect of metformin on the inflammatory response in BV-2 microglial cells induced by lipopolysaccharide (LPS) and S100 calcium-binding protein A8 (S100A8). The results revealed that metformin significantly attenuated several inflammatory responses in BV-2 microglial cells, including the secretion of pro-inflammatory cytokines, such as tumor necrosis factor-${\alpha}$ and interleukin (IL)-6, involved in the activation of Beclin-1, a crucial regulator of autophagy. In addition, metformin inhibited the LPS-induced phosphorylation of ERK. Metformin also suppressed the activation of NOD-like receptor pyrin domain containing 3 inflammasomes composed of NLRP3, caspase-1, and apoptosis-associated speck like protein containing a caspase recruitment domain, which are involved in the innate immune response. Notably, metformin decreased the secretion of S100A8-induced IL-6 production. These findings suggest that metformin alleviates the neuroinflammatory response via autophagy activation.

• The Korea Journal of Herbology
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• v.33 no.5
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• pp.73-79
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• 2018

Objectives : Coriandrum sativum is a medicinal herb that is used to enhance organoleptic quality and food flavor and as source of natural antioxidants. This research investigated the anti-inflammatory activity of Coriandrum sativum stem methanol extract (CSSE) using RAW 264.7 cells. Methods : Production of tumor necrosis factor-${\alpha}$(TNF-${\alpha}$), interleukin (IL)-$1{\beta}$, IL-6, and nitric oxide (NO) in the culture supernatant, protein expression of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and nuclear factor-kappa B (NF-${\kappa}B$) in the extract were assayed. Results : Treatment with CSSE ($100{\mu}g/m{\ell}$) resulted in inhibited levels of protein expression of lipopolysaccharide- (LPS-) induced iNOS, COX-2, and NF-${\kappa}B$ as well as production of TNF-${\alpha}$, IL-$1{\beta}$, IL-6, and NO induced by LPS. Conclusions : These results demonstrate that CSSE exhibits anti-inflammatory activities via decreasing production of pro-inflammatory mediators through suppression of the pathways of NF-${\kappa}B$ in LPS-induced RAW 264.7 cells. Thus, CSSE may have therapeutic potential for a variety of inflammation-mediated diseases.

• Proceedings of the Plant Resources Society of Korea Conference
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• 2021.04a
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• pp.56-56
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• 2021

Nypa fruticans Wurmb is a mangrove plant belonging to Araceae family. N. fruticans is typically found in Southeast Asia, and in some parts of Queensland, Australia. N. fruticans has phytochemicals, phenolics, and flavonoids. In this study, we investigated the anti-inflammatory effects of the ethyl acetate fraction of N. fruticans (ENF) on the production and expression of cytokines and inflammatory mediators through the major signal transduction pathways. ENF attenuated the level of cytokines in a dose-dependent manner and decreased the production of nitric oxide (NO). ENF decreased the expression of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) via alleviating transcription of nuclear factor-kappa B (NF-κB) by an inhibitor of nuclear factor-kappa B (IκB) degradation. Furthermore, mitogen-activated protein kinase (MAPK) signaling pathways (ERK1/2, JNK1/2, and p38) are known to be involved in the inflammatory response. Phosphorylations of ERK1/2, JNK1/2, and p38 were significantly decreased compared with the ENF-untreated control. Conclusively, ENF was related to alleviating various pro-inflammatory mediators through IκB/NF-κB and MAPK signaling pathways, including p65 translocation to the nucleus.

• The Korean Journal of Food And Nutrition
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• v.27 no.6
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• pp.1141-1146
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• 2014

The purpose of this study is to investigate the effects of arabinoxylan rice bran and endurance exercise training on TLR4 mediated protein expression in LPS-treated rats. The results showed that TLR4 as an important protein in the inflammatory response against lipopolysaccharide was shown to be significantly lower in both arabinoxylan supplement with exercise group and exercise group, thus the arabinoxylan rice bran had a higher inhibitory activity than arabinoxylan supplement group. However, $NF-{\kappa}B$ and MyD88 protein expression was not changed in arabinoxylan supplement with exercise training group, whereas $NF-{\kappa}B$ significantly decreased in 4 weeks of exercise training group. These results suggest that the supplement of arabinoxylan rice bran with exercise is likely to contribute to inflammation response and the arabinoxylan rice bran can be used as a possible safe alternative to the immunotherapeutic intervention.

• Biomedical Science Letters
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• v.26 no.1
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• pp.47-50
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• 2020

Recently, decades of robust researches on degenerative brain disorder have been highlighted on the interactive connection of gut and brain. In terms of inflammatory cytokine production, others have shown that Nucleotide-Binding Oligomerization Domain Containing 2 (NOD2) is involved with Leucine-Rich Repeat Kinase 2 (LRRK2). HEK293T cells were transiently co-transfected with Myc-tagged LRRK2 and Flag-tagged NOD2 and then followed by co-immunoprecipitation assay. In this study, we provide the novel finding of physical protein-protein interaction between NOD2 and LRRK2. G2019S variant has shown stronger interactions against NOD2 than those of wild type LRRK2. In an axis of NOD2-LRRK2 communication, it is believed to pave a new way in the understanding of the bidirectional molecular mechanism of brain disorder, including Parkinson's disease into gut inflammatory disease, including Crohn's disease.

• Fisheries and Aquatic Sciences
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• v.21 no.6
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• pp.15.1-15.9
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• 2018

Background: Inflammation has been known to associate with many human diseases. The objective of this study was to evaluate an anti-inflammatory effect of ozonated krill (Euphausia superba) oil, which was prepared by the treatment of krill oil using ozone gas. The anti-inflammatory activity was evaluated in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages. Results: Ozonated krill oil significantly inhibited nitric oxide (NO) production and suppressed the mRNA and protein expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in LPS-stimulated RAW 264.7 macrophages. Ozonated krill oil also reduced the mRNA expression of inflammatory cytokines such as interleukin (IL)-$1{\beta}$, IL-6, and tumor necrosis factor (TNF)-${\alpha}$ in LPS-stimulated RAW 264.7 macrophages. To elucidate the mechanism underlying the anti-inflammatory activity of ozonated krill oil, we evaluated the effects of ozonated krill oil on the activation of mitogen-activated protein kinases (MAPKs) pathway. Ozonated krill oil suppressed the LPS-stimulated phosphorylation of p38 MAPK and c-Jun N-terminal kinases (JNK). Conclusion: This study revealed that the ozonated krill oil exhibited an anti-inflammatory effect in LPS-stimulated RAW 264.7 macrophages. To the best of our knowledge, this is the first report that ozonated krill oil suppressed pro-inflammatory mediator and cytokine expression in LPS-stimulated RAW 264.7 macrophages by inhibiting the phosphorylation of p38 MAPK and JNK.

• Journal of Microbiology and Biotechnology
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• v.29 no.7
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• pp.1022-1032
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• 2019

Probiotics are known to provide the host with immune-modulatory effects and are therefore of remarkable interest for therapeutic and prophylactic applications against various disorders, including inflammatory diseases. Weissella cibaria JW15 (JW15) has been reported to possess probiotic and antioxidant properties. However, the effect of JW15 on inflammatory responses has not yet been reported. Therefore, the objective of the current study was to evaluate the anti-inflammatory potential of JW15 against lipopolysaccharide (LPS) stimulation. The production of pro-inflammatory factors and the cellular signaling pathways following treatment with heat-killed JW15 was examined in LPS-induced RAW 264.7 cells. Treatment with heat-killed JW15 decreased nitric oxide and prostaglandin $E_2$ production via down-regulation of the inducible nitric oxide synthase and cyclooxygenase-2. In addition, treatment with heat-killed JW15 suppressed the expression of pro-inflammatory cytokines, interleukin $(IL)-1{\beta}$, IL-6, and tumor necrosis factor-${\alpha}$. The anti-inflammatory properties of treating with heat-killed JW15 were associated with mitogen-activated protein kinase signaling pathway-mediated suppression of nuclear factor-${\kappa}B$. These results indicated that JW15 possesses anti-inflammatory potential and provide a molecular basis regarding the development of functional probiotic products.