• Title/Summary/Keyword: cyclooxygenase-1

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Inhibitory Effects on the Enzymes Involved in the Inflammation by the Ethanol Extracts of Plant Foodstuffs (식물성 일반식품 자원의 에탄올 추출물이 염증 효소계에 미치는 영향)

  • Kwon, Eun-Sook;Kim, Il-Rang;Kwon, Hoon-Jeong
    • Korean Journal of Food Science and Technology
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    • v.39 no.3
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    • pp.348-352
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    • 2007
  • Inflammation is a complex process resulting from a variety of mechanisms. Combined inhibition of the activities of enzymes involved in the process may therefore be considered more important in anti-inflammatory property of plant extracts than any single contribution. In this study, the inhibitory effects of the ethanol extracts of thirty plant foods on the activities of secretory phospholipase $A_{2}$ ($sPLA_{2}$), cyclooxygenase-1 (COX-1), cyclooxygenase-2 (COX-2), and 12-lipoxygenase (12-LOX) were examined. Several legumes, mungbean sprout and some leaf vegetables inhibited the activity of $sPLA_2$, upstream enzyme of inflammation pathway. Only soybean sprout and mungbean sprout significantly inhibited 12-LOX activity. Although most of extracts inhibited the activities of both COX-1 and COX-2, water dropwort and amaranth showed selectivity for the inhibition of COX-2 over COX-1. Especially, mungbean showed anti-inflammatory property at both upstream and downstream of inflammation pathway with relatively low $IC_{50}$ values for $sPLA_{2}$ and COX-2 enzymes. Mungbean sprout exhibited inhibitory effects on all enzymes related to early and late inflammation and soybean sprout suppressed 12-LOX and COX-2 simultaneously, although the activities of these plants were showed at relatively high concentration. Therefore, mungbean, mungbean sprout, and soybean sprout appear to exhibit anti-inflammatory effects by combined inhibition of inflammatory enzymes.

Synergistic Effects of Exemestane and Aspirin on MCF-7 Human Breast Cancer Cells

  • Hu, Li-Xia;Du, Ying-Ying;Zhang, Ying;Pan, Yue-Yin
    • Asian Pacific Journal of Cancer Prevention
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    • v.13 no.11
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    • pp.5903-5908
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    • 2012
  • Objective: The purpose of this study is to investigate the combined effects of exemestane and aspirin on MCF-7 human breast cancer cells. Methods: Antiproliferative effects of exemestane and aspirin, alone and in combination, on growth of MCF-7 human breast cancer cells were assessed using the MTT assay. Synergistic interaction between the two drugs was evaluated in vitro using the combination index (CI) method. The cell cycle distribution was analyzed by flow cytometry and Western blotting was used to investigate the expression of cyclooxygenase-1, cyclooxygenase-2 and Bcl-2. Results: MTT assays indicated that combination treatment obviously decreased the viability of MCF-7 human breast cancer cells compared to individual drug treatment (CI<1). In addition, the combination of exemestane and aspirin exhibited a synergistic inhibition of cell proliferation, significantly arrested the cell cycle in the $G_0/G_1$ phase and produced a stronger inhibitory effect on COX-1 and Bcl-2 expression than control or individual drug treatment. Conclusion: These results indicate that the combination of exemestane and aspirin might become a useful method to the treatment of hormone-dependent breast cancer. The combination of the two inhibitors significantly increased the response as compared to single agent treatment, suggesting that combination treatment could become a highly effective approach for breast cancer.

Neuroprotective Effect of N-nitro-L-arginine Methylester Pretreatment on the Early Stage of Kainic Acid Induced Neuronal Degeneration in the Rat Brain

  • Koh, Jun-Seok;Kim, Gook-Ki;Lim, Young-Jin;Rhee, Bong-Arm;Kim, Tae-Sung
    • Journal of Korean Neurosurgical Society
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    • v.38 no.4
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    • pp.287-292
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    • 2005
  • Objective : Kainic acid[KA] enhances the expression of nitric oxide synthase, increases nitric oxide[NO], and thus evokes epileptic convulsion, which results in neuronal damage in the rat brain. NO may stimulate cyclooxygenase type-2 [COX-2] activity, thus producing seizure and neuronal injury, but it has also been reported that KA-induced seizure and neurodegeneration are aggravated on decreasing the COX-2 level. This study was undertaken to investigate whether the suppression of NO using the NOS inhibitor, N-nitro-L-arginine methyl ester[L-NAME], suppresses or enhances the activity of COX-2. Methods : Silver impregnation and COX-2 immunohistochemical staining were used to localize related pathophysiological processes in the rat forebrain following KA-induced epileptic convulsion and L-NAME pretreatment. Post-injection survival of the rat was 1, 2, 3days and 2months, respectively. Results : After the systemic administration of KA in rats, neurodegeneration increased with time in the cornu ammonis [CA] 3, CA 1 and amygdala, as confirmed by silver impregnation. On pretreating L-NAME, KA-induced neuronal degeneration decreased. COX-2 enzyme activities increased after KA injection in the dentate gyrus, CA 3, CA 1, amygdala and pyriform cortex, as determined by COX-2 staining. L-NAME pretreatment prior to KA-injection, caused COX-2 activities to increase compared with KA- injection only group by 1day and 2days survival time point. Conclusion : These results suggest that L-NAME has a neuroprotective effect on KA-induced neuronal damage, especially during the early stage of neurodegeneration.

The skin protective effects of compound K, a metabolite of ginsenoside Rb1 from Panax ginseng

  • Kim, Eunji;Kim, Donghyun;Yoo, Sulgi;Hong, Yo Han;Han, Sang Yun;Jeong, Seonggu;Jeong, Deok;Kim, Jong-Hoon;Cho, Jae Youl;Park, Junseong
    • Journal of Ginseng Research
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    • v.42 no.2
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    • pp.218-224
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    • 2018
  • Background: Compound K (CK) is a ginsenoside, a metabolite of Panax ginseng. There is interest both in increasing skin health and antiaging using natural skin care products. In this study, we explored the possibility of using CK as a cosmetic ingredient. Methods: To assess the antiaging effect of CK, RT-PCR was performed, and expression levels of matrix metalloproteinase-1, cyclooxygenase-2, and type I collagen were measured under UVB irradiation conditions. The skin hydrating effect of CK was tested by RT-PCR, and its regulation was explored through immunoblotting. Melanin content, melanin secretion, and tyrosinase activity assays were performed. Results: CK treatment reduced the production of matrix metalloproteinase-1 and cyclooxygenase-2 in UVB irradiated NIH3T3 cells and recovered type I collagen expression level. Expression of skin hydrating factors-filaggrin, transglutaminase, and hyaluronic acid synthases-1 and -2-were augmented by CK and were modulated through the inhibitor of ${\kappa}B{\alpha}$, c-Jun N-terminal kinase, or extracellular signal-regulated kinases pathway. In the melanogenic response, CK did not regulate tyrosinase activity and melanin secretion, but increased melanin content in B16F10 cells was observed. Conclusion: Our data showed that CK has antiaging and hydrating effects. We suggest that CK could be used in cosmetic products to protect the skin from UVB rays and increase skin moisture level.

Ethanol Extract of Oenanthe javanica Modulates Inflammatory Response by Inhibiting NF-${\kappa}B$ Mediated Cyclooxygenase-2 Expression in RAW 264.7 Macrophage

  • Lee, Jeong-Min;Kim, Nam-Joo;Cho, Dong-Hyeok;Chung, Min-Young;Hwang, Kwon-Tack;Kim, Hyun-Ji;Jun, Woo-Jin;Park, Chang-Soo
    • Food Science and Biotechnology
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    • v.15 no.2
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    • pp.303-307
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    • 2006
  • Effect of Oenanthe javanica ethanol extract (OJE) on nuclear factor-${\kappa}B$ (NF-${\kappa}B$)-mediated inflammatory reaction in RAW 264.7 macrophage cells was investigated. The OJE dose-dependently inhibited secretions of tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$) and prostaglandins $E_2\;(PGE_2)$ from lipopolysaccharide (LPS)-stimulated RAW 264.7 cells and blocked LPS-induced expression of cyclooxygenase-2. To clarify mechanistic basis for its inhibitions of NF-${\kappa}B$ and activator protein-1 (AP-1) activations, effects of OJE on activations of NF-${\kappa}B$ and AP-1 genes by luciferase reporter activity were examined. The LPS-stimulated activations of NF-${\kappa}B$ and AP-1 were significantly blocked by 400 and $600\;{\mu$}g/mL of OJE, implicating that OJE might regulate gene expression through more than one signaling pathway. Cytosolic degradation of I-${\kappa}B{\alpha}$ was inhibited by OJE dose-dependently, indicating that the nuclear translocation of p65 was inhibited by OJE. These findings suggest that the inhibition of LPS-stimulated COX-2 expression by OJE is due to its inhibition of NF-${\kappa}B$ activation by blocking I-${\kappa}B{\alpha}$ degradation, which may be mechanistic basis of anti-inflammatory effects of OJE.

The Study of Sagunja-tang, Ijin-tang, Yukgunja-tang on the Change of Cerebral Hemodynamics in Rats (사군자탕, 이진탕, 육군자탕이 뇌혈류역학변동에 미치는 실험적 연구)

  • Jeong Hyun Woo;Kim Hee Seong
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.18 no.1
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    • pp.75-83
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    • 2004
  • This experimental study was designed to investigate the effects of Sagunja-tang(SGJT), Ijin-tang(IJT), Yukgunja-tang(YGJT) on the change of cerebral hemodynamics [regional cerebral blood f1ow(rCBF), mean arterial blood pressure(MABP), and pial arterial diameter (PAD)] in normal rats, and further to determine the mechanism of action of YGJT. And, this Study was designed to investigate whether YGJT inhibit lactate dehydrogenase(LDH) activity in neuronal cells. The results were as follows ; 1. SGJT significantly increased rCBF but MABP was not changed comparing with normal MABP(l00 %). This results were suggested that SGJT significantly increased rCBF by dilating PAD. 2. IJT significantly decreased rCBF in a dose-dependent, but significantly increased MABP in a dose-dependent. This results were suggested that IJT significantly decreased rCBF by contracting PAD. 3. YGJT significantly increased rCBF and PAD in a dose-dependent, and YGJT increased MABP compared with normal MABP(100 %). This results were suggested that YGJT significantly increased rCBF by dilating PAD. 4. The YGJT-induced increase in rCBF was significantly accelerated by pretreatment with indomethacin (IDN, 1 mg/kg, i.p.), an inhibitor of cyclooxygenase but was significantly inhibited by methylene blue (MTB, 10 ㎍/㎏ i.p.), an inhibitor of guanylate cyclase. 5. The YGJT-induced increase in PAD and MABP were accelerated by pretreatment with IDN but was significantly inhibited by MTB. This results suggested that the mechanism of YGJT is mediated by guanylate cyclase. 6. YGJT inhibited significantly LDH activity in neuronal cells. This results were suggested that YGJT prevented the neuronal death. I thought that YGJT should have improvement of cerebral hemodynamics and inhibitive effect on the brain damage.

Bee Venom Suppresses Ischemia-induced Increment of Apoptosis and Cell Proliferation in Hippocampal Dentate Gyrus

  • Lim Baek Vin;Lee Choong Yeol;Kang Jin Oh;Kim Chang Ju;Cho Sonhae
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.18 no.1
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    • pp.236-242
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    • 2004
  • Cerebral ischemia resulting from transient or permanent occlusion of cerebral arteries leads to neuronal cell death and eventually causes neurological impairments. Bee venom has been used for the treatment inflammatory disease. In the present study, the effects of bee venom on apoptosis and cell proliferation in the hippocampal dentate gyrus following transient global ischemia in gerbils were investigated using immunohistochemistry for cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2), caspase-3, and 5-bromo-2'-deoxyuridine (BrdU). It was shown that apoptotic cell death and cell proliferation in the hippocampal dentate gyrus were significantly increased following transient global ischemia in gerbils and that treatment of bee venom suppressed the ischemia-induced increase in apoptosis and cell proliferation in the dentate gyrus. The present results also showed that 1 mg/kg bee-venom treatment suppressed the ischemia-induced increasing apoptosis, cell proliferation, and COX-2 expression in the dentate gyrus. It is possible that the suppression of cell proliferation is due to the reduction of apoptotic cell death by treatment of bee venom. In the present study, bee venom was shown to prosses anti-apoptotic effect in ischemic brain disease, and this protective effect of bee venom against ischemia-induced neuronal cell death is closely associated with suppression on caspase-3 expression.

Study on the Anti-inflammatory Effect and Mechanism of Prunus mume Extract Regarding NF-κB (NF-κB 조절을 통한 오매추출물의 항염효과 및 작용기작에 관한 연구)

  • Seo, Won-Sang;Oh, Han-Na;Park, Woo-Jung;Um, Sang-Young;Lee, Dae-Woo;Kang, Sang-Mo
    • KSBB Journal
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    • v.29 no.1
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    • pp.50-57
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    • 2014
  • NF-${\kappa}B$ is a transcriptional factor which is involved in many biological processes including immunity, inflammation, and cell survival. Many investigators studied on the mechanism involved in activation of NF-${\kappa}B$ signalling pathway via ubiquitination and degradation of $I{\kappa}B$ regarding skin disease. Some specific molecules including Akt, MEK, p38 MAP Kinase, Stat3, et al. represent convergence points and key regulatory proteins in signaling pathways controlling cellular events such as growth and differentiation, energy homeostasis, and the response to stress and inflammation. Ultraviolet (UV) irradiation has many adverse effects on skin, including inflammation, alteration in the extracellular matrix, cellular senescence, apoptosis and skin cancer. Prunus mume, a naturally derived plant extract, has beneficial biological activities as blood fluidity improvement, anti-fatigue action, antioxidative and free radical scavenging activities, inhibiting the motility of Helicobacter pyolri. Previous reports on various beneficial function prompted us to investigate UVB-induced or other immunostimulated biological marker regarding P. mume extract. P. mume extract suppresses UVB-induced cyclooxygenase-2 (COX-2) expression in mouse skin epidermal JB6 P+ cells. The activation of activator protein-1 and nuclear factor-${\kappa}B$ induced by UVB was dose-dependently inhibited by P. mume extract treatment. This results suggest that P. mume extracts might be used as a potential agents for protection of inflammation or UVB induced skin damage.

The Study on Anti-Oxidant and Anti-Inflammatory Effects of Wolbigachul-tang (월비가출탕(越婢加朮湯)의 항산화 및 항염증 효과에 대한 연구)

  • Seung-Kyu Im;Jae-Uk Sul;Seon-Jong Kim;Jae-Min Jeong;Yun-Gwon Seon;Jin-Bong Choi
    • Journal of Korean Medicine Rehabilitation
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    • v.33 no.1
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    • pp.1-12
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    • 2023
  • Objectives This study was conducted to find out the antioxidant and inflammatory improvement effects of Wolbigachul-tang. Methods To evaluate the antioxidant and anti-inflammatory effects of wolbigachul-tang, the total polyphenol and flavonoid contents were measured. And radical scavenging function was measured. In addition reactive oxygen species, nitric oxide, cytokines productions were measured by treating wolbigachul-tang in the lipopolysaccharide-induced RAW264.7 cells. We also measured the gene expression of inducible nitric oxide synthase, cyclooxygenase-2, cytokines too. Results Radical scavenging experiments showed significant concentration-dependent scavenging capacity increase. The amount of reactive oxygen species, nitric oxide, cytokines production in the cell all showed a significant concentration-dependent decrease compared to the control group. The gene expression of inducible nitric oxide synthase, cyclooxygenase-2, and cytokines also showed a significant concentration-dependent decrease compared to the control group. Conclusions In conclusion, it is believed that wolbigachul-tang can be applied to various inflammatory diseases.

The Effect of Ginseng Saponins on the Biosynthesis of Prostaglandins (인삼 Saponin이 Prostaglandin 대사에 미치는 영향)

  • Park C.W.;Lee S.H.
    • Proceedings of the Ginseng society Conference
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    • 1988.08a
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    • pp.77-80
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    • 1988
  • The effects of ginseng saponins and some phenolic acids on the in vitro biosynthesis of prostaglandins was examined in order to identify the role of some ginseng components on the regulaion of arachidonic acid metabolism. The productions of prostaglandin $E_2(PGE_2).$ prostaglandin $F_2{\alpha}(PGF_2{\alpha}).$ thromboxane $B_2(TxB_2)$ and 6-keto-prostaglandin $F_1{\alpha}(6-keto-PGF_1{\alpha})$ from $[^3H]-arachidonic$ acid were evaluated with rabbit kidney microsome. human platelet homogenate and bovine aortic microsome. The amounts of the total cyclooxy-genase products from arachidonic acid did't show significant changes in the presence of ginseng saponins. Panaxadiol. panaxatriol and all of the ginsenosides used in these experiments reduced the formation of $TxB_2.$ while increased the $6-keto-PGF_1{\alpha}$ production dose dependently. Ginseng saponins did't inhibit the ADP($10{\mu}M$) induced platelet aggregation. but sodium arachidonate (0.5 mM) induced platelet aggregation. but sodium arachidonate (0.5 mM) induced platelet aggregation was signiticantly inhibited. These findings suggest that ginseng saponins seem to playa role in the regulation of the arachidonate metabolism. probably by affecting the divergent biosynthetic pathway of prostaglandins from endoperoxide.

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