• The Journal of Internal Korean Medicine
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• v.21 no.4
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• pp.535-542
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• 2000

The water extracts of Samul-tang(SMT) has been used for treatment of ischemic brain damage in Oriental traditional medicine. However, little is known about the mechanism by which the water extracts of SMT rescues brain cells from ischemic damages. To elucidate the protective mechanism on ischemic induced cytotoxicity, I investigate the regulation of LPS and PMA induced iNOS expression in C6 glial cells. LPS and PMA treatment for 72 h in C6 glial cells markedly induce nitric oxide(NO), but treatment of the cells with the water extracts of SMT decrease. dose dependently nitrite formation. In addition, LPS and PMA treatment for 72 h induce severe cell death and LDH release in C6 glial cells. However treatment of the cells with the water extracts of SMT dose not induce significant changes compare to control cells. Furthermore, the protective effects of the water extracts of SMT is mimicked by treatment of $N^{G}MMA$, a specific inhibitor of NOS. LPS and PMA induced iNOS activation in C6 glial cells cause chromosomal condensation and fragmentation of nuclei by caspase activation. The treatment of the cells with the water extracts of SMT may suppress apoptosis via caspase inhibition by regulation of iNOS expression. Taken together, I suggest that the protective effects of the water extracts of SMT against ischemic brain damages may be mediated by regulation of iNOS during ischemic condition.

• Biomedical Science Letters
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• v.24 no.2
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• pp.102-107
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• 2018

Toll-like receptors (TLRs) play an important role for host defense against invading pathogens. The activation of TLRs signaling leads to the activation of $NF-{\kappa}B$ and the expression of pro-inflammatory gene products such as cytokines and inducible nitric oxide synthase (iNOS). To evaluate the therapeutic potential of cardamonin, which is a naturally occurring chalcone from Alpinia species (zingiberaceous plant species), $NF-{\kappa}B$ activation and iNOS expression induced by MALP-2 (TLR2 and TLR6 agonist) or LPS (TLR4 agonist) were examined. Cardamonin inhibited the activation of $NF-{\kappa}B$ induced by MALP-2 or LPS. Cardamonin also suppressed the iNOS expression induced by MALP-2 or LPS. These results suggest that cardamonin has the specific mechanism for anti-inflammatory responses by regulating of TLRs signaling pathway.

• The Journal of Korean Medicine Ophthalmology and Otolaryngology and Dermatology
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• v.21 no.2
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• pp.46-53
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• 2008

Background and Objectives : The aim of this study was to investigate the anti-oxidant, anti-allergic and anti-inflammatory ability of the Taglisodog-eum(SHE) extract on the RAW 264.7 and EL4 cells Materials and Methods : Three types of experiments were implemented for this study: first, the experiment to study the anti-oxidant effect of SHE using Riboflavin; second, in vitro experiment to investigate the inhibition of Th 2 cell differentiation by SHE using EL4 cells (IL-4 mRNA expression); third, the suppression of $NF-{\kappa}B$ activation using RAW 264.7 cells (iNOS and COX-2 mRNA expression). Results : The anti-oxidant ability of SHE were dose-dependantly increased. From in vitro, the LPS-induced iNOS and COX-2 mRNA expression were dose-dependantly decreased in the RAW264.7 cells treated with SHE and the PMA-induced IL-4 mRNA expression were also dose-dependantly decreased in EL4 cells. $NF-{\kappa}B$ activation was suppressed, and iNOS & COX-2 production were inhibited by SHE Conclusion : The results suggest that SHE has dose-dependant anti-oxidant ability, and has anti-allergic and anti-inflammatory effects through the suppression of $NF-{\kappa}B$ activation and the inhibition of Th 2 cell differentiation.

• Molecules and Cells
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• v.26 no.1
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• pp.48-52
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• 2008

We here demonstrate an anti-inflammatory action of raloxifene, a selective estrogen receptor modulator, in lipopolysaccharide (LPS)-induced murine macrophage RAW264.7 cells. Treatment with raloxifene at micromolar concentrations suppressed the production of nitric oxide (NO) by down-regulating expression of the inducible nitric oxide synthase (iNOS) gene in LPS-activated cells. The decreased expression of iNOS and subsequent reduction of NO were due to inhibition of nuclear translocation of transcription factor NF-${\kappa}B$. These effects were significantly inhibited by exposure to the phosphatidylinositol 3-kinase (PI 3-kinase) inhibitor, LY294002, or by expression of a dominant negative mutant of PI 3-kinase. In addition, pretreatment with raloxifene reduced LPS-induced Akt phosphorylation as well as NF-${\kappa}B$ DNA binding activity and NF-${\kappa}B$-dependent reporter gene activity. Thus our findings indicate that raloxifene exerts its anti-inflammatory action in LPS-stimulated macrophages by blocking the PI 3-kinase-Akt-NF-${\kappa}B$ signaling cascade, and eventually reduces expression of pro-inflammatory genes such as iNOS.

• Proceedings of the Korean Environmental Health Society Conference
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• 2005.06a
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• pp.303-305
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• 2005

3-Monochloro-1,2-propanediol (3-MCPD) is a contaminant of acid-hydrolyzed vegetable protein. Several reports have suggested that chronic exposure to 3-MCPD could produce neurotoxicity in vitro or neurobehavioral effects inaspects of experimental animals. Disturbance of the nitric oxide signaling pathway by chronic exposure to 3-MCPD may be a causal factor of neurological disorders in rats. In order to investigate the relationship between 3-MCPD administration and expression of inducibal nitric oxide synthase (iNOS), the numbers and distribution patterns of iNOS-immunoreactive neurons were examined. At the all three bregma level examined, the optical density of iNOS-postive neurons was significantly increased following exposure to 3-MCPD. The change was more severe in the upper layer than in deep layer of the cortex. These data suggest that 3-MCPD toxicity may be mediated through disturbances to the nitric oxide signaling pathway.

• The Korea Journal of Herbology
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• v.27 no.3
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• pp.83-88
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• 2012

Objects : This study was performed in order to observe the effects of water extract of Dendrobii herba on intracerebral hemorrhage(ICH), Method : ICH was induced by the stereotaxic intrastriatal injection of bacterial collagenase type IV in Sprague-Dawley rats. After the water extracts of Dendrobii herba were administrated orally once a day for 3 days, hematoma volume, percentage of brain edema, expression of iNOS and MPO were observed using immunohistochemistry. Results : Rats fed with water extracts of Dendrobii herba showed reduction of hematoma volume and percentage of brain edema compared with controls. In addition, Infiltration of myeloperoxidase (MPO) expressing neutrophil and expression of inducible nitric oxide synthatase(iNOS) were significantly reduced in rats fed with water extracts of Dendrobii herba. Conclusion : These results demonstrated that water extracts of Dendrobii herba reduced brain damage of intracerebral hemorrhage(ICH) and subsequent ICH-induced cerebral edema, and inhibited neutrophil infiltration.

• Journal of Society of Preventive Korean Medicine
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• v.6 no.2
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• pp.147-155
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• 2002

The musk has been reported to have significant anti-inflammatory activities in clinical use and several animal models and we examined the effects of water soluble fraction(WSF) of the musk on murine peritoneal macrophages. WSF decreased the production of nitric oxide from the lipopolysaccharide(LPS)-treated murine peritoneal macrophages and also reduced the phagocytic activity of macrophages on the opsonized sheep red blood cells(SRBC). Transcriptional expression level of the inducible nitric oxide synthase(iNOS) was also decreased and the viability of the treated macrophages was not affected by WSF, suggesting that the effects could be partly explained by transcriptional regulation. Contrary to down-regulating iNOS expression, WSF slightly increased the release of tumor necrosis factor-alpha$(TNF-{\alpha})$, which implied its selective action on cellular pathways activated by LPS. Our results showed that anti-inflammatory activities of the musk could be partly explained by the inhibitory effects of the water soluble fraction on the macrophageal activation.

• Natural Product Sciences
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• v.18 no.3
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• pp.147-152
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• 2012

Ergosta-4,6,8(14),22-tetraen-3-one (1), ergosta-7,24(28)-dien-3-ol (2), and 5,8-epidioxyergosta-6,22-dien-3-ol(3) were isolated from the fruit body of Phellinus pini. Their structures were based on spectroscopic methods including IR, MS, and NMR (1D and 2D). These compounds were screened for their ability to inhibit nitric oxide (NO) production in LPS-activated RAW 264.7 cells. Compounds 1, 2, and 3 reduced NO production in the assay with $IC_50$ values of 29.7 ${\mu}M$ (1), 15.1 ${\mu}M$ (2), and 18.4 ${\mu}M$ (3) respectively. They also suppressed the expression of protein and m-RNA of iNOS and COX-2 in a dose dependent manner by western blot analysis and RT-PCR experiment in LPS-activated microglial cells.

• Proceedings of the PSK Conference
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• 2003.10b
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• pp.151.3-152
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• 2003

Aromatic diamine JSH-21 showed an IC50 value of 9.2 uM with 74.5% inhibition at 30 uM, 53.5% at 10 uM and 24.5% at 3 uM on LPS-induced NO production in murine macrophages Raw 264.7. To examine whether inhibitory effect on NO production by JSH-21 was attributed to influence on iNOS expression, iNOS transcript and protein were analyzed by sequantitative RT-PCR and immunoblot analysis. Consistent with previous result on NO production, treatment of the Raw 264.7 cells with JSH-21 decreased the LPS-induced expression of iNOS transcript and protein in a dose-dependent manner with IC50 values of about 10 uM. (omitted)

• Proceedings of the PSK Conference
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• 2002.10a
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• pp.313.1-313.1
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• 2002

Nitric oxide (NO) production through the inducible nitric-oxide synthase (iNOS) pathway has been implicated in inflammatory diseases and cellular injury. Inhibition of various genes related to inflammation, including iNOS is one of the major roles of well-known anti-inflammatory drugs. In the present study, the effects of ceramide analogs on iNOS expression and NO production were evaluated to investigate how ceramide and its structurally related analogs modulate NO-mecliated cellular signals and inflammation. (omitted)