• Title/Summary/Keyword: Anti TNF

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Anti-dermatitis Effects of KamiCheongsimyeonjatang on GATA-3 Regulation in NC/Nga Mouse (NC/Nga 생쥐에서 가미청심연자탕(加味淸心蓮子湯)의 GATA-3 조절에 의한 항아토피 피부염 효과)

  • Park, Seul-Ki;Han, Jae-Kyung;Kim, Yun-Hee
    • The Journal of Pediatrics of Korean Medicine
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    • v.23 no.2
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    • pp.29-50
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    • 2009
  • Objectives : The purpose of this study is to investigate effectiveness of KamiCheongsimyeonjatang(KCSYJT) medicines to suppress atopic dermatitis in mouse model experimentally. Methods : First, in vitro, we isolated B cells from 18 weeks of atopicdermatitis-like skin NC/Nga mouse. Then we analyzed FACS(Fluorescence Activated Cell Sorter) by intracellular staining of IFN-$\gamma$, GATA-3+ analyzed cytokines by using real-time PCR. Secondly, in vivo, after administration of KCSYJT to atopic dermatitis NC/Nga mouse at 12 weeks of age, we analyzed serum IgE and the change of activated cell in PBMCs(Peripheral Blood Mononuclear Cells). Results : In vitro, KCSYJT medicines supressed IL-1$\beta$, IL-6, TNF-$\alpha$, and TGF-$\beta$ mRNA and increased IL-10 mRNA in B cells. Also, KCSYJT medicines decreased the levels of GATA-3$^+$CD4$^+$ and increased the levels of IFN-$\gamma^+$CD4$^+$T Cell. In vivo, serum IgE levels dreased in KCSYJT group than control group and In PBMCs, the activated cell percentage of granulocytes, CD3+, CD3+/CD4+, B220+/CD23+, and CCR3+ decreased and CD19+, CD3+/CD8+ increased in KCSYJT group than control group. Conclusions : This study demonstrates immunological activity of KCSYJT on atopic dermatitis-like model mice.

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Inhibitory Effects of Black-red Ginseng Extracts on Allergic Inflammation In Vitro and In Vivo (In Vitro 및 In Vivo 알러지성 염증반응에 대한 흑홍삼의 억제효과)

  • Yeom, Mijung;Oh, Ju-Young;Lee, Bombi;Hahm, Dae-Hyun;Park, Hi-Joon
    • Korean Journal of Pharmacognosy
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    • v.48 no.1
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    • pp.38-45
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    • 2017
  • Black-red ginseng (BRGP) exhibits more potent biological activities than white and red ginseng. However, the effect of BRGP on allergic inflammation has not been studied extensively. In this study, we attempted to evaluate the effects of BRGP on allergic inflammation in vitro and in vivo. The effects of BRGP on pro-inflammatory mediators in phorbol myristate acetate (PMA) and A23187-stimulated human mast cells (HMC-1) and on trimellitic anhydride (TMA)-induced atopic dermatitis-like skin lesions in BALB/c mice were evaluated. BRGP suppressed the expression of $TNF-{\alpha}$, IL-6 and IL-8 from HMC-1 stimulated with PMA and A23187. Furthermore, the oral administration of BRGP markedly significantly reduced apparent severity of atopic dermatitis-like skin lesions, ear swelling, lymph node weight gains and serum IgE levels induced by TMA in mice. BRGP treatment also ameliorated epidermal hyperplasia and infiltration of inflammatory cells including mast cells. Taken together, BRGP possesses significant anti-atopic efficacy, suggesting that it could be used as a potential therapeutic agent for allergic inflammatory diseases, including atopic dermatitis.

Effects of Sayeok-tang on Papain-Induced Osteoarthritis in Mice (Papain으로 유도된 골관절염 생쥐 모델에서 사역탕(四逆湯)의 항골관절염 효능에 관한 연구)

  • Kung, Shyang En;Oh, Min Seok
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.27 no.2
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    • pp.212-224
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    • 2013
  • This study intends to clarify how Sayeok-tang(here in after reffered to SYT) affect C57BL/10 mice whose osteoarthritis was induced by papain. Osteoarthritis was induced by injecting papain in the knee joint of 3 groups(n=6) of mice. Normal group was non-treatment group and was not injected papain, whereas control mice were orally administered with $200{\mu}{\ell}$ of physiological saline. Positive comparison group was medicated with 100 mg/kg of Joins$^{(R)}$ mixed with $200{\mu}{\ell}$ of physiological saline. Experimental group was medicated with 400 mg/kg of SYT mixed with $200{\mu}{\ell}$ of physiological saline. Both Positive and experimental comparison groups were orally medicated once per day for 4 weeks. After the experiment, the functions of liver and kidney, inflammation cytokine values within serum, degree of revelation for inflammation cytokine genes, immune cells within blood, metabolism of arachidonic acid and amount of cartilage were measured and histopathological changes in the knee joint structures were observed. As results, SYT had no significant effect on the liver and kidney functions. Interleukin-$1{\beta}$(IL-$1{\beta}$), interleukin-6(IL-6), monocyte chemo attractant protein-1(MCP-1) and tumor necrosis factor-${\alpha}$(TNF-${\alpha}$) were significantly decreased. Inflammation cytokines in joints were all significantly decreased. Prostaglandin $E_2(PGE_2)$, thromboxane $B_2(TXB_2)$ were significantly decreased. Destruction of cartilage on micro computed tomography(CT)-arthrography was meaningfully decreased. In terms of histopathology, infiltration of inflammation, proliferation of synovial membrane, subsidence of cartilage and bone due to penetration of excessive formation of synovial cell and destruction of cartilage were small. Based on all results mentioned above, Sayeok-tang(SYT) is believed to be meaningful for suppressing the progress of osteoarthritis and its treatments because of its anti-inflammatory effects and alleviation of pain with histopathological effective efficacy.

Smilax guianensis Vitman Extract Prevents LPS-Induced Inflammation by Inhibiting the NF-κB Pathway in RAW 264.7 Cells

  • Kim, Ju Gyeong;Kim, Min Jeong;Lee, Ji Su;Sydara, Kongmany;Lee, Sangwoo;Byun, Sanguine;Jung, Sung Keun
    • Journal of Microbiology and Biotechnology
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    • v.30 no.6
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    • pp.822-829
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    • 2020
  • Nutraceutical treatments can reduce inflammation and prevent the development of inflammatory diseases. In this study, the anti-inflammatory effects of Smilax guianensis Vitman extract (SGE) were examined. SGE suppressed lipopolysaccharide (LPS)-mediated nitrite production in RAW 264.7 cells. SGE also prevented the LPS-induced expression of inducible nitric oxide synthase (iNOS) but not cyclooxygenase (COX)-2. Western blot analysis showed that SGE attenuated LPS-induced phosphorylation of IκB kinase (IKK), inhibitor of kappa B (IκB), and p65. Additionally, SGE inhibited LPS-induced IκB degradation in RAW 264.7 cells. Western blot analysis of the cytosolic and nuclear fractions, as well as immunofluorescence assay results, revealed that SGE suppressed LPS-induced p65 nuclear translocation in RAW 264.7 cells. Moreover, SGE reduced LPS-induced interleukin (IL)-1β, IL-6, and tumor necrosis factor-α (TNF-α) mRNA expression and IL-1β and IL-6 protein expression in RAW 264.7 cells. Collectively, these results indicate that SGE suppresses the NF-κB signaling pathway and thereby inhibits the production of NO, IL-1β, and IL-6.

The pistil of nelumbo nucifera has anti-inflammatory effect in LPS-activated Raw 264.7 cells

  • Choi, Woo-Yeon;Jo, Mi-Jeong;Zhao, Rong-Jie;Byun, Sung-Hui;Kim, Mi-Ryeo;Kim, Sang-Chan
    • Herbal Formula Science
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    • v.18 no.1
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    • pp.169-179
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    • 2010
  • The pistil of nelumbo nucifera (PNN) is used in the treatment of nocturnal pollution, hematemesis, epistaxis, metrorrhagia and diarrhoea in traditional medicine. The present study was examined to evaluate the effects of PNN on the production of pro-inflammatory mediators in vitro. After the treatment of PNN, cell viability was measured by MTT assay, nitric oxide (NO) production was monitored by measuring the nitrite content in culture medium. The protein bands were determined by immunoblot analysis and levels of cytokines were analyzed by sandwich immunoassays. In the MTT assay, the doses of PNN extract (0.03, 0.10 mg/ml) had no significant cytotoxicity. The increases of NO production and inducible nitric oxide synthase expression were detected in lipopolysaccharide(LPS)-activated Raw 264.7 cells compared with control, in contrast, these increases were significantly attenuated by pre-treatment with PNN. In cytokine assay, the massive pro-inflammatory cytokines such as tumour necrosis factor-$\alpha$, interleukin (IL)-$1{\beta}$ and IL-6 were induced in LPS-activated Raw 264.7 cells, but pre-treatment of Raw 264.7 cells with PNN caused inhibition (TNF-$\alpha$=14.17%, IL-$1{\beta}$=107.43%, IL-6=46.27%) the production of cytokines by LPS. In addition, PNN reduced prostaglandin E2 productions in a dose-dependent manner (0.03mg/ml=37.52%, 0.10 mg/ml=83.77%) as a consequence of the inhibition of cyclooxygenase-2 expression. Taken together, our data indicates that PNN can regulate the inflammatory response in macrophage cells activated by Gram-negative infection.

Wound Healing Activity of Gamma-Aminobutyric Acid (GABA) in Rats

  • Han, Dong-Oh;Kim, Hee-Young;Lee, Hye-Jung;Shim, In-Sop;Hahm, Dae-Hyun
    • Journal of Microbiology and Biotechnology
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    • v.17 no.10
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    • pp.1661-1669
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    • 2007
  • Gamma-aminobutyric acid (GABA) is a non-protein amino acid. It is well known for its role as an inhibitory neurotransmitter of developing and operating nervous systems in brains. In this study, a novel function of GABA in the healing process of cutaneous wounds was presented regarding anti-inflammation and fibroblast cell proliferation. The cell proliferation activity of GABA was verified through an MTT assay using murine fibroblast NIH3T3 cells. It was observed that GABA significantly inhibited the mRNA expression of iNOS, IL-$1{\beta}$, and TNF-${\alpha}$ in LPS-stimulated RAW 264.7 cells. To evaluate in vivo activity of GABA in wound healing, excisional open wounds were made on the dorsal sides of Sprague-Dawley rats under anesthesia, and the healing of the wounds was apparently assessed. The molecular aspects of the healing process were also investigated by hematoxylineosin staining of the healed skin, displaying the degrees of re-epithelialization and linear alignment of the granulation tissue, and immunostaining and RT-PCR analyses of fibroblast growth factor and platelet-derived growth factor, implying extracellular matrix synthesis and remodeling of the skin. The GABA treatment was effective to accelerate the healing process by suppressing inflammation and stimulating re-epithelialization, compared with the epidermal growth factor treatment. The healing effect of GABA was remarkable at the early stage of wound healing, which resulted in significant reduction of the whole healing period.

Lipoteichoic Acid from Lactobacillus plantarum Inhibits the Expression of Platelet-Activating Factor Receptor Induced by Staphylococcus aureus Lipoteichoic Acid or Escherichia coli Lipopolysaccharide in Human Monocyte-Like Cells

  • Kim, Hangeun;Jung, Bong Jun;Jeong, Jihye;Chun, Honam;Chung, Dae Kyun
    • Journal of Microbiology and Biotechnology
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    • v.24 no.8
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    • pp.1051-1058
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    • 2014
  • Platelet-activating factor receptor (PAFR) plays an important role in bacterial infection and inflammation. We examined the effect of the bacterial cell wall components lipopolysaccharide (LPS) and lipoteichoic acid (LTA) from Lactobacillus plantarum (pLTA) and Staphylococcus aureus (aLTA) on PAFR expression in THP-1, a monocyte-like cell line. LPS and aLTA, but not pLTA, significantly increased PAFR expression, whereas priming with pLTA inhibited LPS-mediated or aLTA-mediated PAFR expression. Expression of Toll-like receptor (TLR) 2 and 4, and CD14 increased with LPS and aLTA treatments, but was inhibited by pLTA pretreatment. Neutralizing antibodies against TLR2, TLR4, and CD14 showed that these receptors were important in LPS-mediated or aLTA-mediated PAFR expression. PAFR expression is mainly regulated by the nuclear factor kappa B signaling pathway. Blocking PAF binding to PAFR using a PAFR inhibitor indicated that LPS-mediated or aLTA-mediated PAF expression affected TNF-${\alpha}$ production. In the mouse small intestine, pLTA inhibited PAFR, TLR2, and TLR4 expression that was induced by heat-labile toxin. Our data suggested that pLTA has an anti-inflammatory effect by inhibiting the expression of PAFR that was induced by pathogenic ligands.

Insulin-like growth factor-1 improves diabetic cardiomyopathy through antioxidative and anti-inflammatory processes along with modulation of Akt/GSK-3β signaling in rats

  • Wang, Cheng Yu;Li, Xiang Dan;Hao, Zhi Hong;Xu, Dongyuan
    • The Korean Journal of Physiology and Pharmacology
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    • v.20 no.6
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    • pp.613-619
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    • 2016
  • Diabetic cardiomyopathy (DCM), a serious complication of diabetes mellitus, is associated with changes in myocardial structure and function. This study sought to explore the ability of insulin-like growth factor-1 (IGF-1) to modulate DCM and its related mechanisms. Twenty-four male Wistar rats were injected with streptozotocin (STZ, 60 mg/kg) to mimic diabetes mellitus. Myocardial fibrosis and apoptosis were evaluated by histopathologic analyses, and relevant proteins were analyzed by Western blotting. Inflammatory factors were assessed by ELISA. Markers of oxidative stress were tested by colorimetric analysis. Rats with DCM displayed decreased body weight, metabolic abnormalities, elevated apoptosis (as assessed by the bcl-2/bax ratio and TUNEL assays), increased fibrosis, increased markers of oxidative stress (MDA and SOD) and inflammatory factors (TNF-${\alpha}$ and IL-$1{\beta}$), and decreased phosphorylation of Akt and glycogen synthase kinase (GSK-$3{\beta}$). IGF-1 treatment, however, attenuated the metabolic abnormalities and myocardial apoptosis, interstitial fibrosis, oxidative stress and inflammation seen in diabetic rats, while also increasing the phosphorylation levels of Akt and GSK-$3{\beta}$. These findings suggest that IGF-1 ameliorates the pathophysiological progress of DCM along with an activation of the Akt/GSK-$3{\beta}$ signaling pathway. Our findings suggest that IGF-1 could be a potential therapeutic choice for controlling DCM.

Therapeutic Profile of T11TS vs. T11TS+MiADMSA: A Hunt for a More Effective Therapeutic Regimen for Arsenic Exposure

  • Chaudhuri, Suhnrita;Acharya, Sagar;Chatterjee, Sirshendu;Kumar, Pankaj;Singh, Manoj Kumar;Bhattacharya, Debanjan;Basu, Anjan Kumar;Dasgupta, Shyamal;Flora, S.J.S.;Chaudhuri, Swapna
    • Asian Pacific Journal of Cancer Prevention
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    • v.13 no.6
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    • pp.2943-2948
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    • 2012
  • Arsenic exposure is a serious health hazard worldwide. We have previously established that it may result in immune suppression by upregulating Th2 cytokines while downregulating Th1 cytokines and causing lymphocytic death. Treatment modalities for arsenic poisoning have mainly been restricted to the use of chelating agents in the past. Only recently have combination therapies using a chelating agent in conjunction with other compounds such as anti-oxidants, micronutrients and various plant products, been introduced. In the present study, we used T11TS, a novel immune potentiating glycopeptide alone and in combination with the sulfhydryl-containing chelator, mono-iso-amyl-dimarcaptosuccinic acid (MiADMSA) as a therapeutic regimen to combat arsenic toxicity in a mouse model. Results indicated that Th1 cytokines such as TNF-${\alpha}$, $IFN{\gamma}$, IL12 and the Th2 cytokines such as IL4, IL6, IL10 which were respectively downregulated and upregulated following arsenic induction were more efficiently restored to their near normal levels by T11TS alone in comparison with the combined regimen. Similar results were obtained with the apoptotic proteins studied, FasL, BAX, BCL2 and the caspases 3, 8 and 9, where again T11TS proved more potent than in combination with MiADMSA in preventing lymphocyte death. The results thus indicate that T11TS alone is more efficient in immune re-establishment after arsenic exposureas compared to combination therapy with T11TS+MiADMSA.

Effect of etoricoxib on experimental oxidative testicular ischemia-reperfusion damage in rats induced with torsion-detorsion

  • Yapanoglu, Turgut;Ozkaya, Fatih;Yilmaz, Ali Haydar;Mammadov, Renad;Cimen, Ferda Keskin;Hirik, Erkan;Altuner, Durdu
    • The Korean Journal of Physiology and Pharmacology
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    • v.21 no.5
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    • pp.457-464
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    • 2017
  • Etoricoxib features antioxidant and anti-inflammatory properties concomitantly, suggesting that it may be beneficial in testicular ischemia reperfusion (I/R) damage. Our aim is to investigate the effects of etoricoxib on testicular I/R damage induced with torsion-detorsion (TD). The etoricoxib + torsion-detorsion (ETD) groups of animals were given etoricoxib in 50 and 100 mg/kg of body weight (ETD-50 and ETD-100), while the testes torsion-detorsion (TTD) and sham operation rat group (SOG) animals were given single oral doses of distilled water as a solvent. TTD, ETD-50 and ETD-100 groups were subjected to $720^{\circ}$ degrees torsion for four hours, and detorsion for four hours. The SOG group was not subjected to this procedure. Biochemical, gene expression and histopathological analyses were carried out on the testicular tissues. The levels of malondialdehyde (MDA), myeloperoxidase (MPO), interleukin-1 beta ($IL-1{\beta}$) and tumor necrosis factor alpha ($TNF-{\alpha}$) were significantly higher, and the levels of total glutathione (tGSH) and glutathione reductase (GSHRd) were significantly lower in the TTD group, compared to the ETD-50, ETD-100 and SOG groups. Etoricoxib at a dose of 100 mg/kg better prevented I/R damage than the 50 mg/kg dose. Etoricoxib may be useful in clinical practice in the reduction of I/R damage on testes caused by torsion-detorsion.