• Journal of Acupuncture Research
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• v.21 no.1
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• pp.33-50
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• 2004

Objective: The aim of this study was to investigate anti-ischemic effect of LR1 HT8 Reduction in Acupuncture Methods: I designed to investigate whether LR1 HT8 Reduction in Acupuncture affects cerebral hemodynamics [regional cerebral blood flow(rCBF), pial arterial diameter(PAD), mean arterial blood pressure(MABP)] in normal rats and to make manifest whether LR1 HT8 Reduction in Acupuncture is mediated by cyclooxygenase or guanylate cyclase. The changes of rCBF and MABP were determinated by laser-doppler flowmetry(LDF), and the change of PAD was de terminated by video microscope and width analyzer. Results: The results were as follows; 1. LR1 Reduction in Acupuncture was increased rCBF and PAD, but decreased MABP. 2. HT8 Reduction in Acupuncture was significantly increased rCBF, but decreased MABP, and increased PAD. 3. LR1 HT8 Reduction in Acupuncture was significantly increased rCBF, PAD, but decreased MABP after withdrawing of the needle. This results suggest that LR1 HT8 Reduction in Acupuncture increased significantly rCBF by dilating PAD. 4. Pretreatment with indomethacin(1mg/kg, i,v.) was significantly inhibited LR1 HT8 Reduction in Acupuncture induced increase of rCBF and PAD, but increased LR1 HT8 Reduction in Acupuncture induced decrease of MABP after withdrawing of the needle. 5. Pretreatment with methylene blue($10{\mu}g/kg$, i,v.) was decreased LR1 HT8 Reduction in Acupuncture induced increase of rCBF and PAD, but accelerated LR1 HT8 Reduction in Acupuncture induced decrease of MABP. Conclusions: I suggest that LR1 HT8 Reduction in Acupuncture has an anti-ischemic effect through the improvement of cerebral hemodynamics, and the mechanism is mediated by cyclooxygenase.

• Natural Product Sciences
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• v.18 no.1
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• pp.22-25
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• 2012

Five triterpenoids, epifriedelanol (1), friedelin (2), lupeol (3), ${\beta}$-sitosterol (4), daucosterol (5), and one phenyl propanoids ester, trans-docosanoyl ferulate (6) were isolated from the whole parts of Portulaca oleracea. They were determined using a combination of spectroscopic analyses ($^1H-$, $^{13}C$-NMR, and MS data) and evaluated for their cyclooxygenase inhibitory activity. Compound 6 exhibited inhibitory effect with $IC_{50}$ values of $40.2{\mu}M$ and 1.6 mM on COX-1 and COX-2 activities, respectively.

• Biomolecules & Therapeutics
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• v.21 no.1
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• pp.54-59
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• 2013

In this study, we investigated the effect of (-)-epigallocatechin-3-gallate (EGCG), a major component of green tea catechins from green tea leaves, on activities of cyclooxygenase (COX)-1 and thromboxane synthase (TXAS), thromboxane $A_2$ ($TXA_2$) production associated microsomal enzymes. EGCG inhibited COX-1 activity to 96.9%, and TXAS activity to 20% in platelet microsomal fraction having cytochrome c reductase (an endoplasmic reticulum marker enzyme) activity and expressing COX-1 (70 kDa) and TXAS (58 kDa) proteins. The inhibitory ratio of COX-1 to TXAS by EGCG was 4.8. These results mean that EGCG has a stronger selectivity in COX-1 inhibition than TXAS inhibition. In special, a nonsteroid anti-inflammatory drug aspirin, a COX-1 inhibitor, inhibited COX-1 activity by 11.3% at the same concentration ($50{\mu}M$) as EGCG that inhibited COX-1 activity to 96.9% as compared with that of control. This suggests that EGCG has a stronger effect than that of aspirin on inhibition of COX-1 activity. Accordingly, we demonstrate that EGCG might be used as a crucial tool for a strong negative regulator of COX-1/$TXA_2$ signaling pathway to inhibit thrombotic disease-associated platelet aggregation.

• Journal of Acupuncture Research
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• v.23 no.2
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• pp.61-72
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• 2006

Objectives : Human chondrocytes co-treated with Buthus martensi Karsch herbal acupuncture solution(BMK-HAS) extract produced significantly less NO compared with chondrocytes stimulated with $IL-1{\beta}$ alone Methods : Activation and translocation of and NF-kB DNA binding activity were determined by Western blotting and specific enzyme-linked immunosorbent assay. Results : The inhibition of NO production correlated with the suppression of induction and expression of nuclear factor-kB (NF-kB) and activation protein-1 (AP-1)-dependent gene. BMK-HAS inhibited the activation and translocation of NF-kB to the nucleus, indicating that BMK-HAS inhibits the $IL-1{\beta}-induced$ production of NO in human chondrocytes by interfering with the activation of NF-kB through a novel mechanism. In addition, BMK-HAS reduced prostaglandin E2 (PGE2)production in mouse peritoneal macrophages stimulated with lipopolysaccharide, whereas no influence on the activity of inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2) or cyclooxygenase-1 (COX-1) was observed. My data, therefore, suggest that BMK-HAS may be a therapeutically effective inhibitor of $IL-1{\beta}-induced$ inflammatory effects that are dependent on NF-kB activation in human OA chondrocytes. Conclusion : The results indicate that BMK-HAS exerts anti-inflammatory effects related to the inhibition of neutrophil functions and of NO and PGE2 production, which could be due to a decreased expression of iNOS and COX-2 through the transcription factors NF-kB and AP-1.

• Journal of Acupuncture Research
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• v.24 no.1
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• pp.111-125
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• 2007

Objection : The aim of this study was to investigate anti-ischemic effect of LR1 ${\cdot}$ HT8 ${\cdot}$ HT9 Reinforcement in Acupuncture. Methods : I designed to investigate whether LR1 ${\cdot}$ HT8 ${\cdot}$ HT9 Reinforcement in Acupuncture affects cerebral hemodynamics [regional cerebral blood flow(rCBF), pial arterial diameter(PAD), mean arterial blood pressure (MABP) ] in normal and cerebral ischemia rats by MCA occlusion method, and to make manifest whether LR1 ${\cdot}$ HT8 ${\cdot}$ HT9 Reinforcement in Acupuncture is mediated by cyclooxygenase or guanylate cyclase. The changes of rCBF and MABP were determinated by laser-doppler flowmetry(LDF), and the change of PAD was determinated by video microscope and width analyzer. Results: The results were as follows ; 1. LR1 ${\cdot}$ HT8 ${\cdot}$ HT9 Reinforcement in Acupuncture was significantly increased rCBF, PAD, but decreased MABP after withdrawing of the needle. This results suggest that LR1 ${\cdot}$ HT8 ${\cdot}$ HT9 Reinforcement in Acupuncture induced significantly rCBF by dilating PAD. 2. Pretreatment with indomethacin (1mg/kg, i.v.) was significantly inhibited LR1 ${\cdot}$ HT8 ${\cdot}$ HT9 Reinforcement in Acupuncture induced increase of rCBF and PAD, but increased LR1 ${\cdot}$ HT8 ${\cdot}$ HT9 Reinforcement in Acupuncture induced decrease of MABP after withdrawing of the needle. 3. Pretreatment with methylene blue(10/${\mu}$g/kg, i.v.) was decreased LR1 ${\cdot}$ HT8 ${\cdot}$ HT9 Reinforcement in Acupuncture induced increase of rCBF and MABP, but accelerated LR1 ${\cdot}$ HT8 ${\cdot}$ HT9 Reinforcement in Acupuncture induced decrease of PAD. This results suggest that the mechanism of LR1 ${\cdot}$ HT8 ${\cdot}$ HT9 Reinforcement in Acupuncture is mediated by cyclooxygenase or guanylate cyclase. Conclusion : I suggest that LR1 ${\cdot}$ HT8 ${\cdot}$ HT9 Reinforcement in Acupuncture has an anti-ischemic effect through the improvement of cerebral hemodynamics, and the mechanism IS mediated by cyclooxygenase.

• Journal of Physiology & Pathology in Korean Medicine
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• v.19 no.5
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• pp.1419-1426
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• 2005

This study was carried out to investigate the effects of herbal extracts on the skin inflammatory reactions which use the makeup preparations. In experiment 1, among the herbal ingredients of herbal extracts, ethanol extracts and 1,3-BG(Butylene Glycol) extracts of Galla Rhois showed potent radical scavenging activity, more than 91% at all concentrations, tested by DPPH (1,1-diphenyl-2-picryl-hyrazyl) method. In experiment 2, ethanol extracts of Chrysanthemi Flos, Gardenias Flos, Galla Rhois showed potent inhibitory activity of the lipopolysaccharide-induced nitric oxide(NO) production, more than 87% at $10{\mu}g/m{\ell}$, by the macrophage RAW 246.7 cells. And 1,3-BG extracts of Taraxaci Herbs, Corm Fructus, Galla Rhois showed potent inhibitory activity of nitric oxide production, more than 89% at $10{\mu}g/m{\ell}$. In experiment 3, ethanol extracts of Chrysanthemi Flos, Gardeniae Flos, Galla Rhois showed potent inhibitory effects of cyclooxygenase-II activity, more than 78% at $10{\mu}g/m{\ell}$, by using ELISA kit. And 1,3-BG extracts of Galla Rhois, Carthami Flos, Chrysanthemi Flos, Taraxaci Herba, Corm Fructus showed potent inhibitory effects of cyclooxygenase-II(COX-II) activity, more than 80% at $10{\mu}g/m{\ell}$. Therefore, 1 expect that herbal extracts, especially Galla Rhois may be used as a drug for treatment on skin inflammation and a material of the makeup preparations.

• Journal of Ginseng Research
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• v.44 no.4
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• pp.655-663
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• 2020

Background: Korean Red Ginseng is known to exhibit immune-enhancing and anti-inflammatory properties. The immune-enhancing effects of the nonsaponin fraction (NSF) of Korean Red Ginseng have been studied in many reports. However, the gastroprotective effect of this fraction is not fully understood. In this study, we demonstrate the activities of NSF for gastrointestinal protection and its related critical factor. Methods: The in vitro and in vivo regulatory functions of NSF on cyclooxygenase-1 (COX-1) messenger RNA and protein levels were examined by reverse transcription polymerase chain reaction and immunoblotting analyses. Gastroprotective effects of NSF were investigated by histological score, gastric juice pH, and myeloperoxidase activity on indomethacin-induced, cold stress-induced, and acetylsalicylic acid-induced gastritis and dextran sulfate sodium-induced colitis in in vivo mouse models. Results: NSF did not show cytotoxicity, and it increased COX-1 messenger RNA expression and protein levels in RAW264.7 cells. This upregulation was also observed in colitis and gastritis in vivo models. In addition, NSF treatment in mice ameliorated the symptoms of gastrointestinal inflammation, including histological score, colon length, gastric juice pH, gastric wall thickness, and myeloperoxidase activity. Conclusion: These results suggest that NSF has gastroprotective effects on gastritis and colitis in in vivo mouse models through COX-1 upregulation.

• Biomedical Science Letters
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• v.15 no.2
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• pp.141-146
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• 2009

Paclitaxel, an antimicrotubule agent, binds to beta-tubulin in the microtubule and stabilizes the polymer, thereby repressing dynamic instability. Here, we have demonstrated that microtubule cytoskeletal architecture involved in regulation of the COX-2 expression in chondrocyte treated with paclitaxel. Paclitaxel enhanced COX-2 expression and prostaglandin E2 production, as indicated by the Western blot analysis, reverse transcriptase PCR(RT-PCR) and immunofluorescence staining, and $PGE_2$ assay, respectively. In our previous data have shown that paclitaxel treatment stimulated activation of ERK-1/2 and p38 kinase(Im et al., 2009). SB203580, an inhibitor of p38 kinase, blocked the induction of COX-2 expression by paclitaxel. Also PD98059, an inhibitor of ERK-1/2 kinase was blocked the induced COX-2 expression. These results indicate that activation of ERK-1/2 and p38 kinase is required for COX-2 expression induced by paclitaxel in rabbit articular chondrocytes.

• YAKHAK HOEJI
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• v.43 no.1
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• pp.117-123
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• 1999

Because of the potent effects of lipid mediators such as prostaglandins (PGs), leukotriens (LTs) and platelet activating factor (PAF) on a variety of cells and tissues, they are considered as major contributors to the process leading to inflammation and allergy. To pursue the mechanism of anti-inflammatory activity of Lonicera japonica, we tested inhibitory effects of 7 flavonoids from Lonicera japonica on arachidonic acid cascade related enzymes, such as inflammatory phospholipase $A_2$, cyclooxygenase-1 and 2, 5-lipoxygenase, in bone marrow derived mast cell (BMMC), and lyso PAF-acetyltransferase in rat spleen microsomes. Anti-inflammatory activities of lonicera japonica are thought to be attributed at least in part to the inhibition of arachidonic acid cascade releated enzymes by flavonoids such as apigenin, luteolin quercetin.

• Proceedings of the PSK Conference
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• 2003.10b
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• pp.70.1-70.1
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• 2003

Celecoxib, the selective cyclooxygenase-2 (COX-2) inhibitor, has recently been reported to reduce the formation of polyps in patients with familial adenomatous polyposis. This specific COX-2 inhibitor also protects against experimentally induced carcinogenesis, but molecular mechanisms underlying its chemopreventive activities remain largely unresolved. In the present work, we found that celecoxib inhibited 12-O- tetradecanoylphorbol-13-acetate (TPA)-induced expression of COX-2 in female ICR mouse skin when applied topically 30 min prior to TPA as determined by both immunoblot and immunohistochemical analyses. (omitted)