• Archives of Pharmacal Research
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• v.29 no.7
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• pp.591-597
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• 2006

Aerial parts of Artemisia asiatica (Compositae) have been traditionally used as an oriental medicine for the treatment of inflammatory and ulcerogenic diseases. In the present study, artemisolide was isolated as a nuclear factor $(NF)-{\kappa}B$ inhibitor from A. asiatica by activity-guided fractionation. Artemisolide inhibited $NF-{\kappa}B$ transcriptional activity in lipopolysaccharide (LPS)-stimulated macrophages RAW 264.7 with an $IC_{50}$ value of $5.8\;{\mu}M$. The compound was also effective in blocking $NF-{\kappa}B$ transcriptional activities elicited by the expression vector encoding the $NF-{\kappa}B$ p65 or p50 subunits bypassing the inhibitory kB degradation signaling $NF-{\kappa}B$ activation. The macrophages markedly increased their $PGE_2$ and NO production upon exposure to LPS alone. Artemisolide inhibited LPS-induced $PGE_2$ and NO production with $IC_{50}$ values of $8.7\;{\mu}M$ and $6.4\;{\mu}M$, respectively, but also suppressed LPS-induced synthesis of cyclooxygenase (COX)-2 or inducible NO synthase (iNOS). Taken together, artemisolide is a $NF-{\kappa}B$ inhibitor that attenuates LPS-induced production of $PGE_2$ or NO via down-regulation of COX-2 or iNOS expression in macrophages RAW 264.7. Therefore, artemisolide could represent and provide the anti-inflammatory principle associated with the traditional medicine, A. asiatica.

• Journal of Korean Medicine Rehabilitation
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• v.24 no.4
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• pp.15-28
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• 2014

Objectives This study was carried out to find out the Antioxidant and Anti-inflammatory Effects of Components of Mahwangbujaseshin-tang in LPS-Stimulated RAW264.7 Macrophages. Methods There are 5 experimental groups. ; normal, control, EH (Ephedrae Herba), ALRP (Aconiti Lateralis Radix Preparata) and AR (Asiasari Radix). The extract of EH, ALRP and AR ($100{\mu}g/ml$) was added to each group. We examined cytotoxicity, total phenolic contents, DPPH and ABTS free radical scavenging activity, Intracellular ROS (reactive oxygen species) production, NO (Total Nitric oxide), iNOS (inducible nitric oxide synthase), PGE2 (prostaglandin E2), COX-2 (cyclooxygenase-2), $IL-1{\beta}$ ($interleukin-1{\beta}$), IL-6 (interleukin-6), $TNF-{\alpha}$ (tumor necrosis factor-${\alpha}$), MMP-9 (matrix metalloproteinase-9), TIMP-1 (tissue inhibitor of metalloproteinase-1) and HO-1 (heme oxygenase-1) expression level. Results 1. Total phenolic contents of EH were in the highest level. 2. DPPH and ABTS free radical scavenging activity of EH was in the highest level. 3. ROS production was significantly decreased in AR. 4. NO production was significantly decreased in EH, ALRP, AR and iNOS expression was decreased in EH, AR. 5. PGE2 and COX-2 expression was decreased in EH, AR. 6. $IL-1{\beta}$ production was significantly decreased in EH, AR and IL-6 production was significantly decreased in AR. $TNF-{\alpha}$ production was significantly decreased in ALRP, AR. 7. MMP-9 and TIMP-1 production were significantly decreased in EH. 8. HO-1 expression was significantly increased in EH. 9. With simultaneous usage of SnPP which is expression inhibitor of HO-1, NO, $IL-1{\beta}$, IL-6 and $TNF-{\alpha}$ production were partially increased in EH, ALRP, AR. Conclusions According to this study, Components of Mahwangbujaseshin-tang have anti-oxidants and anti-inflammation effects in LPS-Stimulated RAW264.7 Macrophages.

• Tuberculosis and Respiratory Diseases
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• v.41 no.5
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• pp.513-520
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• 1994

Background: The pathogenesis of silicosis has been focused on the interaction between alveolar macrophages and silica particle. Although fibrosis in silicosis has been studied extensively, the mechanism is still not fully understood. There is increasing evidence that monokines and arachidonic acid metabolites macrophage are involved in pathogenesis of silicosis. Recently, it was reported that prostaglandin E2 produced from macrophage counteracts the stimulatory effects of other monokines on fibroblast proliferation or collagen production. Until now, it was remained uncertain by which mechanism silica particle may activate alveolar macrophage to an enhanced release of prostaglandin E2. Methods: In order to investigate the relationship between the activity of alveolar macrophage and the production of $PGE_2$ from activated alveolar macrophage, the authors measured hydrogen peroxide and $PGE_2$ from alveolar macrophages activated by silica in vitro and from alveolar macrophages in the silicotic nodules from rat. Experimental silicosis was induced by intratracheal infusion of silica($SiO_2$) suspended in saline(50 mg/ml) in Sprague-Dawley rats. Results: produced by 1) The silicotic nodules with fibrosis were seen from the sections of rat lung at 60 days after intratracheal injection with 50 mg aqueous suspension of silica(Fig. 1). 2) In vitro, silica caused the dose dependent increase of hydrogen peroxide(p<0.05, Fig. 2A) and $PGE_2$(p>0.05, Fig. 2B) release from alveolar macrophages. Alveolar macrophages from rat with silicotic nodules released more hydrogen peroxide and $PGE_2$ than those of control group(p<0.05, Fig. 3). Conclusion: These results suggest that silica particle could activate macrophage directly and enhanced the release of $PGE_2$ and hydrogen peroxide from the alveolar macrophage.

• Herbal Formula Science
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• v.16 no.1
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• pp.79-94
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• 2008

Although inflammatory mediators such as nitric oxide(NO) and pro-inflammatory cytokines are involved in host defense mechanism, these overproduction contributes to the pathogenesis of several diseases such as otitis media, hearing loss, periodontitis, bacterial sepsis, rheumatoid arthritis, chronic inflammation and autoimmune diseases. We investigate the anti-inflammatory effects of water extract from Ji-Pae-San(JPSWE) fomulated with Angelica dahurica plus Fritillaria Verticillata, Angelica dahurica(ADWE), and Fritillaria Verticillata(FUVE) in vitro and in vivo. Each extract inhibited the production of inflammatory mediators(NO, $IL-1{\beta}$, IL-6, $TNF-{\alpha}$, and prostaglandin $E_2$) and the expression of inducible NO synthase(iNOS) and cyclooxygenase-2(COX-2) in lipopolysaccharide(LPS)-stimulated RAW 264.7 macrophages in a dose-dependent manner. These inhibitory effects were synergistically increased by their combination. JPSWE also inhibited $TNF-{\alpha}$, $IL-1{\beta}$, IL-6. and $PGE_2$ production as well as COX activity in LPS-stimulated mice. Moreover, JPSWE significantly suppressed death by LPS-septic shock in mice(survival rate: 100%). These results suggest that Ji-Pae-San may be useful for therapeutic drugs against inflammatory immune diseases, probably by suppressing the production of inflammatory mediators.

• Journal of Physiology & Pathology in Korean Medicine
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• v.22 no.4
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• pp.878-883
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• 2008

Conchiolin is a complex protein which is secreted by the mollusc's outer epithelium to be the organic basis of mollusc shell. This study is to investigate a potential anti-inflammatory activity of conchiolin of oyster shell (COS). We tested the effects of COS on the lipopolysaccharide (LPS)-induced production of nitric oxide (NO) and prostaglandin E2 (PGE 2) in a murine macrophage cell line, RAW 264.7. COS inhibited production of NO and PGE2 in a dose dependent manner and also decreased the expression of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), tumor necrosis $factor-{\alpha}$ ($TNF-{\alpha}$) and interleukin-6 (IL-6). These results suggest that COS can inhibit production of pro-inflammatory mediators and might be a useful source to treat inflammation.

• Korean Journal of Pharmacognosy
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• v.37 no.4 s.147
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• pp.283-289
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• 2006

Ethanol extracts of the whole herb of Agastachis Herba (A) and of Pueraria Radix (P) alone and of their mixture (A+P) downregulated the cell growth, cyclooxygenase-2 (COX-2) expression, prostaglandin $E_2\;(PGE_2)$, and cGMP production. A, P, and A + P inhibited the cell growth of HT-29 colon cancer cells in a concentration- and time-dependent manner but not the growth of normal colon cell, CCD-112CoN. In addition, they markedly inhibited the productions of $PGE_2$ and cGMP as well as the mRNA expression of COX-2. These data suggest that non-toxic concentration of A, P, and A + P have a significant effect on the in vitro growth of HT-29 cells, specifically through the inhibition of the $PGE_2$ production via COX-2.

• The Journal of Pediatrics of Korean Medicine
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• v.21 no.2
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• pp.97-107
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• 2007

Objectives This experiment is about Jojoongikgi-tang(JIT) exerts anti-inflammatory effects in BV2 microglial cells, and the effect of JIT on Nitric oxide(NO) production in lipopolysaccharide(LPS)-stimulated BV2 microglial cells were also demonstrated. Methods To investigate the anti-inflammatory effects of JIT, NO production, expression level of iNOS mRNA, PGE2 synthesis, expression COX-2 mRNA, cell viability, $TNF-{\alpha}$ mRNA expression were examined. Results The expression level of inducible nitric oxide synthase(iNOS) was decreased by JIT, and the production of Prostaglandin E2(PGE2) and the expression of Cox-2 mRNA also were inhibited by JIT. Proinflammatory mediators, such as $TNF-{\alpha}$, $IL-1{\beta}$, IL-12, were inhibited by JIT in a dose-dependent manner. Conclusions JIT have anti-inflammatory effects in BV2 microglial cells and could be used in inflammatory disease.

• YAKHAK HOEJI
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• v.50 no.2
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• pp.99-104
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• 2006

Prostaglandins biosynthesis and nitric oxide production have been implicated in the process of inflammation. In this study we investigated on the effects of ethyl acetate extract of Angelica Koreana Radix (EAKR) on the activities of prostaglandin $E_2\;(PGE_2)$, proteoglycan (PG) degradation and nitric oxide synthase (NO) in inflammation cytokines-activated rabbit articular chondrocytes. EAKR exhibited inhibitory activities on NO production and $PGE_2$ production as $73.08\%\;and\;89.49\%$, respectively at $20{\mu}g/ml$ and inhibited the degradation of PG in a concentration-dependent manner Zelatin zymography analysis demonstrated that EAKR significantly inhibited MMP-2, 9 expression in chondrocytes. In vivo, EAKR was shown to have inhibitory effects on acetic acid-induced pain. This study suggests that modulation of $PGE_2$, NO, PG degradation and MMP-2, 9 by EARK may be important in the prevention of inflammation and osteroarthritis.

• Korean Journal of Oriental Medicine
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• v.14 no.3
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• pp.57-63
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• 2008

Glehnia littoralis (Umbelliferae) is the medicinal plant used traditionally for treatment of immune-related diseases. Prostaglandins and nitric oxide (NO) have been implicated as important mediators in the processes of inflammation and carcinogenesis. For understanding the mechanisms for pharmacological activities of Glehnia littoralis, we evaluated the inhibitory activity of Glehnia littoralis on lipopolysaccharide (LPS)-induced prostaglandin $E_2$ ($PGE_2$) and NO production in mouse macrophage RAW264.7 cells. The results showed that the extract of Glehnia littoralis inhibited LPS- induced $PGE_2$ production effectively, but not NO. Additional study revealed that the extract of Glehnia littoralis suppressed cyclooxygenase-2 (COX-2) expression in a dose-dependent manner. Present study suggests that Glehnia littoralis may have anti-inflammatory and/or cancer chemopreventive activity through the inhibition of $PGE_2$ production by the suppression of COX-2 activity.

• Fisheries and Aquatic Sciences
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• v.6 no.3
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• pp.130-134
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• 2003

Proinflammatory effects of bacterial lipopolysaccharide (LPS) have been assessed by analysing the induction of two inflammatory genes, $interleukin-1\beta$ $(IL-1\beta)$ and cyclooxygenase-2 (COX-2), in rainbow trout (Oncorhynchus mykiss) macrophage cells. Production of a metabolite of arachidonic acid by COX-2, prostaglandin $E_2\;(PGE_2)$, was also analysed in macrophage cells after LPS stimulation. Northern blot analysis revealed that LPS $(5{\mu}g/mL)$ significantly upregulated $IL-1\beta$ (54 times) and COX-2 (40.7 times) gene expression in macrophage cells after 4 h stimulation. According to RT-PCR (Reverse Transcription Polymerase Chain Reaction) analysis, $IL-1\beta$ gene induction in LPS stimulated macrophage cells was started within 1h and significantly increased thereafter until 4h. Meanwhile, COX-2 gene induction by LPS was delayed in comparison with $IL-1\beta$ gene induction as a faint band was observed after 4h stimulation in head kidney macrophage cells. LPS also significantly increased $PGE_2$ production in head kidney leucocytes, presumably via activating COX-2 expression that metabolites arachidonic acid to $PGE_2$. In conclusion, it was demonstrated that LPS could induce two main inflammatory and immune related genes, $IL-1\beta$ and COX-2, and increase $PGE_2$ production in trout head kidney macrophage cells, representing a strong inflammatory activity.