• Title/Summary/Keyword: anti-inflammation action

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Phosphorylation of Akt Mediates Anti-Inflammatory Activity of 1-p-Coumaroyl ${\beta}$-D-Glucoside Against Lipopolysaccharide-Induced Inflammation in RAW264.7 Cells

  • Vo, Van Anh;Lee, Jae-Won;Kim, Ji-Young;Park, Jun-Ho;Lee, Hee Jae;Kim, Sung-Soo;Kwon, Yong-Soo;Chun, Wanjoo
    • The Korean Journal of Physiology and Pharmacology
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    • v.18 no.1
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    • pp.79-86
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    • 2014
  • Hydroxycinnamic acids have been reported to possess numerous pharmacological activities such as antioxidant, anti-inflammatory, and anti-tumor properties. However, the biological activity of 1-p-coumaroyl ${\beta}$-D-glucoside (CG), a glucose ester derivative of p-coumaric acid, has not been clearly examined. The objective of this study is to elucidate the anti-inflammatory action of CG in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophage cells. In the present study, CG significantly suppressed LPS-induced excessive production of pro-inflammatory mediators such as nitric oxide (NO) and $PGE_2$ and the protein expression of iNOS and COX-2. CG also inhibited LPS-induced secretion of pro-inflammatory cytokines, IL-$1{\beta}$ and TNF-${\alpha}$. In addition, CG significantly suppressed LPS-induced degradation of $I{\kappa}B$. To elucidate the underlying mechanism by which CG exerts its anti-inflammatory action, involvement of various signaling pathways were examined. CG exhibited significantly increased Akt phosphorylation in a concentration-dependent manner, although MAPKs such as Erk, JNK, and p38 appeared not to be involved. Furthermore, inhibition of Akt/PI3K signaling pathway with wortmannin significantly, albeit not completely, abolished CG-induced Akt phosphorylation and anti-inflammatory actions. Taken together, the present study demonstrates that Akt signaling pathway might play a major role in CG-mediated anti-inflammatory activity in LPS-stimulated RAW264.7 macrophage cells.

Inhibitory Effects of Water Extract of Lindera obtusiloba on the Mast Cell-Mediated Allergic Inflammation (생강나무 추출물의 알레르기성 염증반응 억제 효과)

  • Kim, Sang-Hyun;Son, Jun-Ho;Lee, Seung-Ho
    • Korean Journal of Pharmacognosy
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    • v.40 no.3
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    • pp.233-237
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    • 2009
  • Lindera obtusiloba has been used for centuries as a traditional medicine in Korea and recently known to have an anti-fibrotic effect. In this report, we investigated the effect of hot water extract from L. obtusiloba (WELB) on the mast cell-mediated allergic inflammation and studied its possible mechanisms of action. WELB inhibited phorbol-12-myristate 13-acetate and calcium ionophore A23187 (PMACI)-induced histamine release in HMC-1 human mast cells. WELB reduced PMACI-induced gene expression and secretion of proinflammatory cytokines such as tumor necrosis factor-$\alpha$, interleukin (IL)-$1{\beta}$, IL-6, and IL-8. The inhibitory effect of WELB on the expression of proinflammatory cytokines was c-jun N-terminal kinase and nuclear factor-${\kappa}B$ dependent. These results indicate that WELB may be beneficial in the treatment of mast cell-mediated allergic inflammation.

The various mechanisms of Korean traditional medicines for anti-cancer (한약의 다양한 항암기전)

  • Park, Yeong-Chul;Park, Yong-Ki;Lee, Sun-Dong
    • The Korea Journal of Herbology
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    • v.27 no.3
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    • pp.39-55
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    • 2012
  • Objectives : Recently there have been encouraging results, from a western perspective, in the cancer research field regarding the anticancer effects of herbal medicine. This paper was aimed to review herbal medicine playing its anticancer role in terms of apoptosis, inflammation control, differentiation and telomerase. Methods : New studies for tang, medicinal herb itself or effective ingradients of medicinal herb showing anti-cancer effectiveness were reviewed and summarized in terms of pharmacological action. Results : Ethanol extracts of $Spatholobus$ $suberectus$ greatly inhibited cancer cell growth inducing cell apoptosis and cytotoxic effects. $Scutellaria$ $baicalensis$ may be responsible for its anticancer activity showing inhibition of $PGE_2$ synthesis via suppression of COX-2 expression. Saikosaponins isolated from $Bupleurum$ induced the differentiation of C6 glioma cells, cancer cells, into astrocytes, normal cells. Acetone extract of $Bupleurum$ $scorzonerifolium$ inhibited proliferation of human lung cancer cells via inducing apoptosis and suppressing telomerase activity. Conclusions : Herbal medicine inhibited cancer cell growth inducing cell apoptosis and cytotoxic effects. Inflammation persisting for a decade eventually elevates the risk of cancer sufficiently that it is discernible in case control epidemiological studies. Differentiation therapy is defined as a therapy to treat cancers by inducing differentiation of the stem cells. Telomerase expression is a hallmark of cancer. Nearly the complete spectrum of human tumors has been shown to be telomerase positive.

Anti-Anaphylactic Effects of Natural Extract Compounds(AllerQ) in the Rats (천연물 복합체가 추출물(알러큐)의 알러지 유발 흰쥐에 대한 항알러지 효과)

  • Suh Kyong-Suk;Kwon Myung-Sang;Cho Jung-Soon
    • Journal of the East Asian Society of Dietary Life
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    • v.14 no.5
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    • pp.425-437
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    • 2004
  • Medicinal plants are of great importance in providing healthcare to a large portion of the population in Korea. A number of plants are described in Dong-Ui-Bo-Gam for use in the treatment of allergic disorders, namely psoriasis, eczema, bronchial asthma, etc. In this study, we evaluated the effect of AllerQ, which is multi-complexes of various plants extracts such like Mori folium, Scutellaria baicallensis, Glycyrrhiza uralnsis, Mentha sacharinensis and Poncirus trifoliata on compound 48/80 induced anaphylactic shock, ovalbumin induced asthma in vivo and anti-IgE antibody induced hypersensitivity in vitro. We found antianaphylactic or antiallergic properties of AllerQ when given orally. AllerQ for prophylactic treatment for anaphylactic shocks have produced good results. AllerQ may modulate various aspects of immune function and allergic inflammation. In the present study, we analyse the effects of AllerQ on mast cell degranulation, mortality, cAMP/cGMP, O₂, H₂O₂ level, cyokine production and on the elicitation of IgE-mediated mast cell-dependent allergic inflammation in vivo and in vitro. We have established that AllerQ inhibited histamine release, cAMP/cGMP, O₂, H₂O₂ level, IL-4, tumor necrosis factor-alpha(TNF-α) and IL-6 production without having any significant physical change. These effects have been observed in mast cell(in vitro) and serum(in vivo) derived from three different origins that were activated by either immunological or non-immunological stimuli. These results suggest that the antianaphylactic and antiasthma tic action of AllerQ may be associated with an increase in the intracellular inhibition of the cAMP phosphodiesterase. Furthermore, AllerQ identified as potent inhibitors on O₂, H₂O₂ and cytokine activity. these data suggest that AllerQ may have an inhibitory role in mast cell-mediated allergic inflammation, and thus might be considered as an useful functional food.

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Gold Sodium Thiomalate Inhibits iNOS Gene Expression in RAW 264.7 Macrophage: Differential Regulation by Gold Sodium Thiomalate and Sodium Salicylate (Gold Sodium Thiomalate에 의한 유도성 Nitric Oxide Synthase Gene의 발현억제: Gold 제제와 Sodium Salicylate의 차이점)

  • 임종호;배진영
    • Biomolecules & Therapeutics
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    • v.10 no.4
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    • pp.230-235
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    • 2002
  • Gold sodium thiomalate (GST, gold compound) is a widely used anti-arthritic, anti-rheumatic and anti-inflammatory drug that is considered a good alternative to sodium salicylate (NaSA) for individuals who cannot tolerate salicylates. Nitric oxide (NO) synthesized by inducible nitric oxide synthase (iNOS) has been implicated as a mediator of inflammation. Recent evidence suggests that anti-inflammatory effect of NaSA lies in the inhibition of iNOS, but nothing has been reported about the direct effect of iNOS expression by GST. The present study was designed to elucidate sequentially the action mechanisms of GST and NaSA on lipopolysaccharide (LPS) plus interferon-gamma (IFN-$\gamma$) induced iNOS expression in RAW 264.7 macrophages. Both GST and NaSA inhibited NO production and iNOS protein expression in a dose dependent manner. GST inhibited iNOS mRNA expression induced by LPS plus IFN-$\gamma$, whereas NaSA did not. These findings suggest that GST may exert anti-arthritic, anti-rheumatic and anti-inflammatory effect by inhibiting iNOS expression induced by LPS plus IFN-$\gamma$ at transcriptional level, whereas NaSA exert its effect by inhibiting iNOS expression at the translational or posttranslational level.

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.

Anti-Inflammatory Principles from the Fruits of Evodia rutaecarpa and Their Cellular Action Mechanisms

  • Choi Yong-Hwan;Shin Eun-Myoung;Kim Yeong-Shik;Cai Xing-Fu;Lee Jung-Joon;Kim Hyun-Pyo
    • Archives of Pharmacal Research
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    • v.29 no.4
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    • pp.293-297
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    • 2006
  • The fruits of Evodia rutaecarpa Benth (Rutaceae) has long been used for inflammatory disorders and some anti-inflammatory actions of its constituents such as dehydroevodiamine, evodiamine and rutaecarpine were previously reported. Since the pharmacological data is not sufficient to clearly establish the scientific rationale of anti-inflammatory medicinal use of this plant material and the search for its active principles is limited so far, three major constituents (evodiamine, rutaecarpine, goshuyuamide II) were evaluated for their anti-inflammatory cellular action mechanisms in the present study. From the results, evodiamine and rutaecarpine were found to strongly inhibit prostaglandin $E_2$ synthesis from lipopolysaccharide-treated RAW 264.7 cells at $1-10{\mu}M$. Evodiamine inhibited cyclooxygenase-2 induction and NF-kB activation, while rutaecarpine did not. On the other hand, goshuyuamide II inhibited 5-lipoxygenase from RBL-1 cells $(IC_{50}=6.6{\mu}M)$, resulting in the reduced synthesis of leukotrienes. However, these three compounds were not inhibitory against inducible nitric oxide synthase-mediated nitric oxide production from RAW cells up to $50{\mu}M$. These pharmacological properties may provide the additional scientific rationale for anti-inflammatory use of the fruits of E. rutaecarpa.

The Root from Heracleum moellendorffii Exerts Anti-Inflammatory Activity via the Inhibition of NF-κB and MAPK Signaling Activation in LPS-Stimulated RAW264.7 Cells

  • Park, Su Bin;Kim, Ha Na;Kim, Jeong Dong;Park, Gwang Hun;Son, Ho-Jun;Eo, Hyun Ji;Song, Jeong Ho;Jeong, Hyung Jin;Jeong, Jin Boo
    • Proceedings of the Plant Resources Society of Korea Conference
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    • 2018.10a
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    • pp.96-96
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    • 2018
  • Although the roots of Heracleum moellendorffii (HM-R) have been long treated for inflammatory human diseases, scientific evidence for the anti-inflammatory activity of HM-R is not sufficient. In this study, we investigated anti-inflammatory activity and mechanism of action of HM-R in LPS-stimulated RAW264.7 cells. HM-R blocked LPS-induced NO and PGE2 production, but not HM-L. HM-R inhibited LPS-induced overexpression of iNOS, COX-2, $IL-1{\beta}$ and IL-6 in RAW264.7 cells. HM-R inhibited LPS-induced $NF-{\kappa}B$ signaling activation through blocking $I{\kappa}B-{\alpha}$ degradation and p65 nuclear accumulation. In addition, HM-R inhibited MAPK signaling activation by attenuating the phosphorylation of ERK1/2, p38 and JNK. Furthermore, HM-R inhibited attenuated LPS-mediated overexpression of the osteoclast-specific factors such as NFATc1, cathepsin K, MCP-1 and TRAP. These results indicate that HM-R may exert anti-inflammatory activity by inhibiting $NF-{\kappa}B$ and MAPK signaling activation. From these findings, HM-R has potential to be a candidate for the development of chemopreventive or therapeutic agents for the inflammation and inflammatory diseases.

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Iontiophoretic Transdermal Delivery of Triamcinolone Acetonide on Delayed Onset Muscle Soreness (지연성 근육통에 대한 Triamcinolone Acetonide의 이온도입 경피투과)

  • Jung, Dae-In;Kim, Myong-Hoon;Hwang, Tae-Yeun;Yoon, Se-Won;Choi, Eun-Young
    • Journal of the Korean Academy of Clinical Electrophysiology
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    • v.1 no.1
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    • pp.45-56
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    • 2003
  • This study investigated the effects of triamcinolone acetonide by iontophoretic transdermal drug delivery on anti-inflammatory action into the human which had excentric exercise-induced delayed onset muscle soreness in the non-dominant arm. The degree of anti-inflammation was evaluated creatine posphokinase(CPK) by serum enzyme activity and subjective pain threshold by soreness muscle scale in clinical study. The results Were as follows; 1. In a subjective pain scale, all groups showed non-significant difference but, showed a tendency to decrease numerical value in human. 2. In the serum CPK level, iontophoresis group showed more significant reduction than other groups at 24, 48 and 72 hours. From the results, the iontophoresis with triamcinolone acetonide is more effective than using each groups. The continuous study is needed for many interesting issues of iontophoretic transdermal drug delivery in new future.

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Aprotinin Inhibits Vascular Smooth Muscle Cell Inflammation and Proliferation via Induction of HO-1

  • Lee, Dong-Hyup;Choi, Hyoung-Chul;Lee, Kwang-Youn;Kang, Young-Jin
    • The Korean Journal of Physiology and Pharmacology
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    • v.13 no.2
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    • pp.123-129
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    • 2009
  • Aprotinin is used clinically in cardiopulmonary bypass surgery to reduce transfusion requirements and the inflammatory response. The mechanism of action for the anti-inflammatory effects of aprotinin is still unclear. We examined our hypothesis whether inhibitory effects of aprotinin on cytokine-induced inducible nitric oxide synthase (iNOS) expression (IL-$l\beta$ plus TNF-$\alpha$), reactive oxygen species (ROS) generation, and vascular smooth muscle cell (VSMC) proliferation were due to HO-l induction in rat VSMCs. Aprotinin induced HO-l protein expression in a dose-dependent manner, which was potentiated during inflammatory condition. Aprotinin reduced cytokine mixture (CM)-induced iNOS expression in a dose dependent manner. Furthermore, aprotinin reduced CM-induced ROS generation, cell proliferation, and phosphorylation of JNK but not of P38 and ERK1/2 kinases. Aprotinin effects were reversed by pre-treatment with the HO-l inhibitor, tin protoporphyrin IX (SnPPIX). HO-l is therefore closely involved in inflammatory-stimulated VSMC proliferation through the regulation of ROS generation and JNK phosphorylation. Our results suggest a new molecular basis for aprotinin anti-inflammatory properties.