• The Korea Journal of Herbology
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• v.28 no.6
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• pp.87-93
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• 2013

Objectives : Degenerative arthritis arises from several physiological factors. The purpose of this study is to investigate the beneficial effects of Phyto-extract Complex (CME) on degenerative arthritis. Methods : CME is composed of extracts of mulberry (Morus alba L.) fruit, mulberry leaves and black beans (Glycine max (L.) Merr.). To measure the toxicity of CME, we performed the single-dose toxicity study. For the evaluation of its effects on degenerative arthritis, we examined the inhibition of cyclooxygenase-2 (COX-2) activity, using in vitro enzyme activity assay, the reduction of protein expression of COX-2, 5-lipoxygenase (5-LO), and inducible nitric oxide synthase (iNOS) in RAW264.7 cells which were stimulated by lipopolysaccharide (LPS). We also examined the serum level of prostaglandins (PGs) and injury of the knee joint cartilage, using animal model of degenerative arthritis induced by mono-sodium iodoacetate (MIA). Results : CME did not have any toxicity in single-dose toxicity study. The CME inhibited the activity of COX-2 and could reduce the protein expression of COX-2, 5-LO and iNOS in RAW264.7 cells. The CME also reduced the serum level of PGs and prevented from the cartilage injury of knee joint in animal model of degenerative arthritis induced by MIA. Conclusions : Taken altogether, the CME could be useful for the improvement of degenerative arthritis through its various anti-inflammatory activities and prevention from the cartilage injury of knee joint.

• Journal of Life Science
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• v.21 no.5
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• pp.678-683
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• 2011

The objective of this study was to evaluate the skin inflammation effects of three herb mixture extracts, Ligularia fischeri, Solidago virga-aurea and Aruncus dioicus, which are from Ullung island in Korea. Regulatory mechanisms of cytokines and nitric oxide (NO) are involved in the immunological activity of Raw 264.7 cells. Tested cells were pretreated with 70% acetone extracts of Ligularia fischeri, Solidago virga-aurea and Aruncus dioicus (LSA-A) and further cultured for an appropriated time after lipopolyssacharide (LPS) addition. During the entire experimental period, 1, 10, and 100 ${\mu}g/ml$ of LSA-A had no cytotoxicity. In these concentrations, LSA-A inhibited the production of NO and prostaglandin $E_2$ ($PGE_2$), tumor necorsis factor-a (TNF-a), interleukin-1${\beta}$ (IL-1${\beta}$), interleukin-6 (IL-6) expression of inducible NO synthase (iNOS), and cyclooxygenase-2 (COX-2). LSA-A showed a 60% $PGE_2$ inhibition rate at 100 ${\mu}g/ml$. iNOS and COX-2 inhibition activities were 54%, and 65% at 100 ${\mu}g/ml$, respectively. In addition, LSA-A extract reduced the release of inflammatory cytokines including TNF-a, IL-1${\beta}$ and IL-6. These results suggest that LSA-A may have significant effects on inflammatory factors, and may be a potential anti-inflammatory therapeutic agent.

• The Korean Journal of Physiology and Pharmacology
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• v.1 no.4
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• pp.393-402
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• 1997

In the present study, we characterized the angiotensin II (AII)-induced relaxations in the phenylephrine-precontracted rabbit mesenteric arteries with endothelium. 1) AII-induced relaxation was consistently observed in the rabbit mesenteric arteries with and without endothelium, but not in the aortic segment with endothelium. 2) AII-induced endothelium-dependent relaxation was markedly inhibited by $N^w-nitro-L-arginine$ (L-NNA, $100\;{\mu}M$), methylene blue ($10\;{\mu}M$) and LY83583 ($10\;{\mu}M$), respectively. 3) Inhibition of cyclooxygenase with indomethacin ($10\;{\mu}M$) strongly decreased the vasorelaxant response to AII irrespective of the presence of endothelium. 4) 7-Ethoxyresorufin ($1\;{\mu}M$) and clotrimazole ($1\;{\mu}M$), inhibitors of cytochrome P-450-dependent arachidonic acid metabolism, greatly attenuated the vasodilator response to AII. 5) Carbacyclin, arachidonic acid and prostaglandin $F_{2{\alpha}}$ ($PGF_{2{\alpha}}$) caused concentration-dependent relaxations in the mesenteric artery with endothelium, which were inhibited by L-NNA and methylene blue. 6) AII and $PGF_{2{\alpha}}$ significantly stimulated cyclic GMP formation in the mesenteric arteries with endothelium, which was inhibited by L-NNA and methylene blue, respectively. 7) AII enhanced synthesis of $PGF_{2{\alpha}}$ and 6-keto $PGF_{1{\alpha}}$ from the arterial segments with endothelium, which was inhibitable by indomethacin, but not by L-NNA. In conclusion, the vasorelaxant responses to AII of the rabbit mesenteric artery with endothelium are subserved by arachidonic acid and its metabolites produced via activation of cyclooxygenase and cytochrome P-450 enzyme as well as by nitric oxide.

• Proceedings of the PSK Conference
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• 2003.04a
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• pp.127.2-128
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• 2003

Rutaecarpine is an alkaloid originally isolated from the unripe fruit of Evodia rutaecarpa. In addition to its traditional use in treatment of gastrointestinal disorders, rutaecarpine has recently been characterized to have anti-inflammatory activity through cyclooxygenase-2 inhibition. More recently, to develop rutaecarpine as an anti-inflammatory agent, total synthesis of rutaecarpine has successfully been established in our group. (omitted)

• Archives of Pharmacal Research
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• v.29 no.8
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• pp.685-690
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• 2006

The effect of a main constituent ginsenoside Rg5 isolated from red ginseng and its metabolite ginsenoside Rh3 in a chronic dermatitis model was investigated. Ginsenosides Rg5 and Rh3 suppressed swelling of oxazolone-induced mouse ear contact dermatitis. These ginsenosides also reduced mRNA expressions of cyclooxygenase-2, interleukin $(IL)-1{\beta}$, tumor necrosis factor $(TNF)-{\alpha}$ and interferon $(IFN)-{\gamma}$. The inhibition of ginsenoside Rh3 was more potent than that of ginsenoside Rg5. These findings suggest that ginsenoside Rh3 metabolized from ginsenoside Rg5 may improve chronic dermatitis or psoriasis by the regulation of $IL-1{\beta}$ and $TNF-{\alpha}$ produced by macrophage cells and of $IFN-{\gamma}$ produced by Th cells.

• Journal of Life Science
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• v.21 no.12
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• pp.1689-1697
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• 2011

In this study, we investigated the anti-inflammation effect of Persicaria thunbergii (P. thunbergii) on RAW 264.7 murine macrophage cells. The anti-inflammatory activity of P. thunbergii was determined by measuring expression of the LPS-induced inflammatory proteins, inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2) and nuclear factor-${\kappa}B$ (NF-${\kappa}B$), and the production of nitric oxide (NO) and prostaglandin $E_2$ ($PGE_2$). Methanol extract of P. thunbergii decreased the expression of iNOS, COX-2 and NF-${\kappa}B$, and increased the expression of HO-1 in LPS-stimulated RAW264.7 cells. Methanol extract was fractioned by n-butanol, hexane and ethyl acetate (EtOAc) and each fraction was tested for inhibitory effects on inflammation. Among the sequential solvent fractions, the EtOAc soluble fraction was investigated by the expression of prostaglandin $E_2$ ($PGE_2$), and showed decreasing form to the dose-dependent manner. EtOAc extract showed the most effective inhibitory activity of the expression of iNOS, COX-2 and NF-${\kappa}B$, and the production of NO. The study showed that P. thunbergii has anti-inflammatory activity through the decrease of NO and inhibition of iNOS, COX-2, $PGE_2$ and NF-${\kappa}B$ expression, and by the increase of HO-1 enzyme. This study needs for more investigation to find out the most effective single compound with anti-inflammatory activity.

• Journal of Ginseng Research
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• v.37 no.1
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• pp.54-63
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• 2013

Ginsenoside Rd is a primary constituent of the ginseng rhizome and has been shown to participate in the regulation of diabetes and in tumor formation. Reports also show that ginsenoside Rd exerts anti-oxidative effects by activating anti-oxidant enzymes. Treatment with ginsenoside Rd decreased nitric oxide and prostaglandin $E_2$ ($PGE_2$) in lipopolysaccharides (LPS)-challenged RAW264.7 cells and in ICR mouse livers (5 mg/kg LPS; LPS + ginsenoside Rd [2, 10, and 50 mg/kg]). Furthermore, these decreases were associated with the down-regulations of inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2 and of nuclear factor (NF)-${\kappa}B$ activity in vitro and in vivo. Our results indicate that ginsenoside Rd treatment decreases; 1) nitric oxide production (40% inhibition); 2) $PGE_2$ synthesis (69% to 93% inhibition); 3) NF-${\kappa}B$ activity; and 4) the NF-${\kappa}B$-regulated expressions of iNOS and COX-2. Taken together, our results suggest that the anti-inflammatory effects of ginsenoside Rd are due to the down-regulation of NF-${\kappa}B$ and the consequent expressional suppressions of iNOS and COX-2.

• Journal of Dental Anesthesia and Pain Medicine
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• v.22 no.4
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• pp.277-287
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• 2022

Background: Inflammatory dental diseases that occur during pregnancy can cause preterm labor and/or intrauterine growth restriction. Therefore, proactive treatment of dental diseases is necessary during pregnancy. Dexmedetomidine (DEX) is a widely used sedative in the dental field, but research on the effect of DEX on pregnancy is currently insufficient. In this study, we investigated the effects of co-treatment with DEX and lipopolysaccharide (LPS) on inflammatory responses in human amnion-derived WISH cells. Methods: Human amnion-derived WISH cells were treated with 0.001, 0.01, 0.1, and 1 ㎍/mL DEX with 1 ㎍/mL LPS for 24 h. Cytotoxicity of WISH cells was evaluated by 3-(4,5-dimethylthiazol)-2,5-diphenyltetrazolium bromide (MTT) assay. The protein expression of cyclooxygenase-2 (COX-2), prostaglandin E₂ (PGE₂), p38, and nuclear factor kappa B (NF-𝜅B) was examined by western blot analysis. The mRNA expression of pro-inflammatory cytokines such as interleukin (IL)-1𝛽 and tumor necrosis factor (TNF)-𝛼 was analyzed by real-time quantitative polymerase chain reaction. Results: Co-treatment with DEX and LPS showed no cytotoxicity in the WISH cells. The mRNA expression of IL-1𝛽 and TNF-𝛼 decreased after co-treatment with DEX and LPS. DEX and LPS co-treatment decreased the protein expression of COX-2, PGE₂, phospho-p38, and phospho-NF-𝛋B in WISH cells. Conclusion: Co-treatment with DEX and LPS suppressed the expression of COX-2 and PGE₂, as well as pro-inflammatory cytokines such as IL-1𝛽 and TNF-𝛼 in WISH cells. In addition, the anti-inflammatory effect of DEX and LPS co-treatment was mediated by the inhibition of p38/NF-𝜅B activation.

• Journal of Life Science
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• v.23 no.1
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• pp.55-62
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• 2013

The objective of this study was to evaluate the anti-inflammation effect of extract of Carthamus tinctorious seed, on skin obtained from Gyeong buk, Korea. Regulatory mechanisms of cytokines and nitric oxide (NO) involved in immunological activity of Raw 264.7 cells. Tested cells were pretreated with 70% ethanol extracted of Carthamus tinctorious seed and further cultured for an appropriated time after the addition of lipopolyssacharide (LPS). During the entire experimental period, 5, 10, 25 and 50 ${\mu}g/ml$ of Carthamus tinctorious seed showed no cytotoxicity. In these concentrations, ethyl acetate layer of ethanol extracted Carthamus tinctorius seed (CT-E/E) inhibited the production of NO and prostaglandin $E_2$ ($PGE_2$), tumor necorsis factor-a (TNF-${\alpha}$), interleukin-$1{\beta}$ (IL-$1{\beta}$), interleukin-6 (IL-6) expression of inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2). At a 50 ${\mu}g/ml$ level of CT-E/E, $PGE_2$, iNOS and COX-2 inhibition activity were shown 60%, 38%, and 42%, respectively. In addition, CT-E/E reduced the release of inflammatory cytokines including TNF-${\alpha}$, IL-$1{\beta}$ and IL-6. These results suggest that Carthamus tinctorious seed extracts may be a potential anti-inflammatory therapeutic agent due to the significant effects on inflammatory factors.

• Journal of Physiology & Pathology in Korean Medicine
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• v.22 no.5
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• pp.1315-1321
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• 2008

Chan-Su (Venenum bufonis) has long been for a variety of other purposes including treatment of inflammation in the folk medicine recipe. Since nitric oxide (NO) is one of the major inflammatory parameters, we first studied the effects of Chan-Su on NO production in lipopolysaccharide (LPS)-stimulated BV2 microglial cells, Chan-Su inhibited the secretion of NO in BV2 microglial cells, without affecting cell viability, The protein level of inducible nitric oxide synthase (iNOS) was decreased by Chan-Su, And Chan-Su also inhibited production of prostaglandin E2 (PGE2) and expression of cyclooxygenase (COX)-2. Proinflammatory cytokines, such as tumor necrosis factor $(TNF)-{\alpha}$, interleukin $(IL)-1{\beta}$ and IL-12, were inhibited by Chan-Su in a dose-dependent manner. And Chan-Su inhibited the degradation of ${IkB-\alpha}$, which was considered to be inhibitor of nuclear factor $(NF)-{\kappa}B$, one of a potential transcription factor for the expression of iNOS, COX-2 and proinflammatory cytokines. These results suggest that Chan-Su could exert its anti-inflammatory actions by suppressing the synthesis of NO through inhibition of $I{\kappa}B-{\alpha}$ degradation.