• Title/Summary/Keyword: ccl4

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Hepatoprotective Effects of Ginseng Intestinal Metabolite IH-901 on Chemical-Induced Hepatic Damage

  • Sohn, Uy-Dong;Ko, Sung-Kwon;Choi, Tae-Sik;Im, Byung-Ok ;Han, Sung-Tai;Yang, Byung-Wook;Sung, Jong-Hwan;Kim, Yong-Sung;Woo, Jae-Gwang;Cho, Young-Rae;Min, Young-Sil;Jeong, Ji-Hoon;Lee, Boo-Yong
    • Food Science and Biotechnology
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    • v.14 no.4
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    • pp.558-560
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    • 2005
  • Hepatoprotective effects of white ginseng extract (WGE), and IH-901 (20-O-${\beta}$-D-glucopyranosyl-20(S)-protopanaxadiol) derived from intestinal metabolite of ginsenoside $Rb_1$ were studied using two experimental animal models with chemical-induced hepatic damage. Administration of WGE (200 and 500 mg/kg) and IH-901 (0.01, 0.05, and 0.1 mM/kg) significantly decreased aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels in acute hepatitic mice induced by $CCl_4$. Administration of WGE (l00 mg/kg) and IH-901 (0.02, 0.04, and 0.08 mM/kg) significantly decreased AST and ALT levels in acute hepatitic rats induced by D-galactosamine. AST and ALT levels of IH-901 groups decreased. These results suggested WGE and IH-901 may have protective effects against chemical-induced hepatic damage.

Candida rugosa Lipase-Catalyzed Production of Optically Pure S-(+)-Ketoprofen (Candida rugosa 리파제를 이용한 광학적으로 순수한 S-(+)-Ketoprofen의 생산)

  • 김민곤;최순자;최원아;김철호;정봉현
    • KSBB Journal
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    • v.14 no.2
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    • pp.225-229
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    • 1999
  • Enzymatic resolution reactions were investigated using Candida rugosa lipase for the production of potically pure S-(+)-Ketoprofen. When the enzymatic hydroysis (and esterification) of recemic ketoprofen esters (and recemic ketoprofen with alcohol) was investigated comparatively, aqueous media was more specific for S-enantiomer than organic media. In the enzymatic hydrolysis of racemic ketoprofen ethyl ester in aqueous media, optimal temperature and pH for enantioselectivity were $37^{\circ}C$ and 4, respectively. The stereoselectivity of the enzyme was enhanced by adding dialcohols such as ethylene glycol and propylene glycol. The enantiomeric ratio obtained in the 40 %(v/v) ethylene glycol was 2-fold higher than that without the additive. By adding $CH_2Cl_2$, $CHCl_3$ and $CCl_4$ (5%,v/v), the enantioselectivity was reversed. A dramatic increase in the stereoselectivity was achieved using lipase purified by anion exchange chromatography. The type A lipase(the first eluted lipase fraction) showed an enantiomeric ratio of >100, whereas the type B lipase(the second eluted lipase fraction) exhibited enantimomer ratio of 9.0 in the hydrolysis of racemic ketoprofen ethyl ester.

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Antioxidant Effects of Sagunja-Tang (Sijunzi-Tang) (사군자탕(四君子湯)의 항산화(抗酸化) 효과(效果))

  • Lee Yong-Tae;Cho Su-In;Kim Young-Kyun
    • Journal of Society of Preventive Korean Medicine
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    • v.4 no.2
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    • pp.170-192
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    • 2000
  • Objectives : This study was carried out to research antioxidant effects of Sagunja-Tang(SA) through in vitro and vivo experiments, and tried to investigate the relation between oxidation of tissues and deficiency of Qi. Methods and results : HPLC analysis of glycyrrhizine - known to be the main compound of Radix Glycyrrhizae - was done to certify the quality of SA. Chemiluminescence was initiated by adding tort-butyl hydroperoxide (t-BHP) to rabbit polymorphonuclear leukocytes (neutrophils), and generated reactive oxygen species (superoxide anion) decreased significantly by SA as dose dependent manner. Cell injury during 60 minutes tissue incubation was initiated by adding t-BHP, a hydrophobic hydroperoxide and $H_2O_2$, an water soluble oxidant to rat renal cortical and liver slices. Percentage cell death and lipid peroxidation were estimated by measuring lactate dehydrogenase (LDH) and malondialdehyde (MDA), a product of lipid peroxidation. t-BHP induced % cell death of renal cortical slices and lipid peroxidation of renal cortical and liver slices were decreased significantly by SA. SA decreased significantly % cell death and lipid peroxidation of renal cortical and liver slices induced by $H_2O_2$, too. Acute renal and liver injury induced by $HgCl_2\;and\;CCl_4$, which initiated from free radical, were applied to mice and metabolic data were obtained. Data showed protective effects of SA on acute renal injury caused by decrease of glomerular filtration. SA protected acute liver injury too. Conclusions Through this study, we found that SA have antioxidant effects and tissue oxidation was similar to deficiency of Qi. And further studies have to be followed to certify the mechanisms.

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The Effect of Additives in Final Rinse Water on Soiling and the Removal of Soil. (세탁후 최종처리액의 조성이 직물의 오염 및 세척성에 미치는 영향)

  • Cho Sung Kyo;Kim Sang Reon
    • Journal of the Korean Society of Clothing and Textiles
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    • v.2 no.1
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    • pp.167-176
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    • 1978
  • The effect of additives in final rinse water during laundering on soiling, soil removal and some properties of fabrics has been studied with various fabrics. The additives examined were fabric softener (Sta-Puf), cationic surfactant (Apole PS), sizing materials such as CMC, PYA, cornstarch and mixture of CMC and cationic surfactant. The results obtained may be summerized as follows. L Addition of additives except PVA in final rinse water generally reduce the deposition of carbon-$CCl_4$ soil and it seems to be rather independant of the concentration of additives. The effect of additives on soil resistant is found to increase in the following order. cotton; Apole

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Inhibition of Tumor Necrosis $Factor-{\alpha}$ mRMA Expression by a Limited Series of Tetrahydroisoquinolines in Mouse Peritoneal Macrophages

  • Jung, Tae-Ho;Lee, Young-Soo;Kang, Young-Jin;Lee, Bog-Kyu;Ko, Young-Shin;Seo, Han-Geuk;Chung, Soo-Youn;Lee, Duck-Hyung;Yun-Choi, Hye-Sook;Chang, Ki-Churl
    • The Korean Journal of Physiology and Pharmacology
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    • v.4 no.4
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    • pp.325-331
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    • 2000
  • Tumor necrosis $factor-{\alpha}\;(TNF-{\alpha})$ plays important roles in inflammatory responses. Some of tetrahydroisoquinoline (THI) compounds exhibited to inhibit iNOS expression in animal studies and RAW 264.7 cells, but the action of THI on inflammatory reaction was not fully investigated. In the present study, we examined a limited series of THIs (higenamine, YS-51 and THI-52) on the $TNF-{\alpha}$ mRNA expression in mouse peritoneal macrophages by Northern analysis. When thioglycollate-stimulated peritoneal macrophages were incubated with LPS (100 ng/ml), expression of $TNF-{\alpha}$ mRNA was evident and reached its maximum at 2.5 h, which was reduced concentration-dependently by treatment with THIs. When the $TNF-{\alpha}$ activity of macrophage-conditioned media was measured using a TNF-sensitive L929 fibroblast cell line, CCL 1, all THIs increased the cell viability in a concentration dependent manner. The concentrations of THIs used are not cytotoxic by itself when analysed by MTT. Furthermore, nitrite/nitrate level was significantly reduced by the presence of THIs in cells treated with $LPS+interferon-{\gamma}\;(IFN-{\gamma}).$ It is concluded, thus, that these results strongly indicated that THIs can suppress the $TNF-{\alpha}$ expression and reduce NO, which may be useful for the inflammatory disorders.

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Microarray Study of Genes Differentially Modulated in Response to Nitric Oxide in Macrophages

  • Nan, Xuehua;Maeng, Oky;Shin, Hyo-Jung;An, Hyun-Jung;Yeom, Young-Il;Lee, Hay-Young;Paik, Sang-Gi
    • Animal cells and systems
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    • v.12 no.1
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    • pp.15-21
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    • 2008
  • Nitric oxide(NO) has been known to play important roles in numerous physiologic processes including neurotransmission, vasorelaxation, and cellular apoptosis. Using a mouse cDNA gene chip, we examined expression patterns and time course of NO-dependent genes in mouse macrophage RAW264.7 cells. Genes shown to be upregulated more than two fold or at least at two serial time points were further selected and validated by RT-PCR. Finally, 81 selected genes were classified by function as signaling, apoptosis, inflammation, transcription, translation, ionic homeostasis and metabolism. Among those, genes related with signaling, apoptosis and inflammation, such as guanylate cyclase 1, soluble, alpha3(Gucy1a3); protein kinase C, alpha($Pkc{\alpha}$); lymphocyte protein tyrosine kinase(Lck); BCL2/adenovirus E1B 19 kDa-interacting protein(Bnip3); apoptotic protease activating factor 1(Apaf1); X-linked inhibitor of apoptosis(Xiap); cyclin G1(Ccng1); chemokine(C-C motif) ligand 4(Ccl4); B cell translocation gene 2, anti-proliferative(Btg2); lysozyme 2(Lyz2); secreted phosphoprotein 1(Spp1); heme oxygenase(decycling) 1(Hmox1); CD14 antigen(Cd14); and granulin(Grn) may play important roles in NO-dependent responses in murine macrophages.

The Pharmacokinetics of Nimodipine After Oral Administration in Rabbits with Hepatic Failure

  • Choi, Jun-Shik;Choi, In;Burm, Jin-Pil
    • Journal of Pharmaceutical Investigation
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    • v.36 no.1
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    • pp.19-22
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    • 2006
  • The pharmacokinetics of nimodipine, following a single 16 mg/kg oral dose, was investigated in rabbits with hepatic failure induced by 0.5 mL/kg (mild), 1.0 mL/kg (moderate) and 2.0 mL/kg (severe) of carbon tetrachloride $(CCl_{4}$ : olive oil = 20 : 80, v/v). The plasma concentrations of nimodipine were determined by a high performance liquid chromatographic assay. The levels of sGOT and sGPT in rabbits with mild $(86.2{\pm}29.0\;and\;98.5{\pm}33.1\;unit/dL)$, moderate $(168.1{\pm}61.2\;and\;196.2{\pm}66.0\;unit/dL)$ and severe $(292.7{\pm}82.2\;and\;314.2{\pm}99.8\;unit/dL)$ hepatic failure were significantly increased compared to the control $(38.0{\pm}10.1\;and\;32.4{\pm}10.2\;unit/dL)$. The area under the plasma concentration-time curve (AUC) of nimodipine was significantly increased in mild $(131.7{\pm}28.1%)$, moderate $(168.8{\pm}32.8%)$ and severe $(204.6{\pm}58.3%)$ carbon tetrachloride-induced hepatic failure rabbits compared to the control (100%) rabbits. The volume of distribution $(V_{d})$ and the total body clearance $(CL_{t})$ of nimodipine were significantly decreased in all hepatic failure groups. The elimination rate constant $(K_{el})$ of nimodipine was significantly decreased in moderate and severe carbon tetrachloride-induced hepatic failure rabbits. There was a correlation between sGOT (y= 1.01x+241, r=0.993) or sGPT (y=0.92x +243, r=0.997) value and the AUC of nimodipine in the rabbits with hepatic failure. These findings suggest that the hepatic metabolism of nimodipine was inhibited by carbon tetrachloride-induced hepatic failure rabbits, resulting in the decrese in $V_{d}$ and $CL_{t}$ of nimodipine in the rabbits with mild, moderate and severe hepatic failure.

Increased Lymphocyte Infiltration in Rheumatoid Arthritis Is Correlated with an Increase in LTi-like Cells in Synovial Fluid

  • Koo, Jihye;Kim, Soochan;Jung, Woong Jae;Lee, Ye Eun;Song, Gwan Gyu;Kim, Kyung-Su;Kim, Mi-Yeon
    • IMMUNE NETWORK
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    • v.13 no.6
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    • pp.240-248
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    • 2013
  • In this study, we compared the immune cell populations in rheumatoid arthritis (RA) synovial fluid, which shows lymphoid tissue-like structure, with those in tonsils, which are normal secondary lymphoid tissues. Firstly, we found that $CD4^-CD11b^+$ macrophages were the major population in RA synovial fluid and that B cells were the major population in tonsils. In addition, synovial fluid from patients with osteoarthritis, which is a degenerative joint disease, contained $CD4^+CD11b^+$monocytes as the major immune cell population. Secondly, we categorized three groups based on the proportion of macrophages found in RA synovial fluid: (1) the macrophage-high group, which contained more than 80% macrophages; (2) the macrophage-intermediate group, which contained between 40% and 80% macrophages; and (3) the macrophage-low group, which contained less than 40% macrophages. In the macrophage-low group, more lymphoid tissue inducer (LTi)-like cells were detected, and the expression of OX40L and TRANCE in these cells was higher than that in the other groups. In addition, in this group, the suppressive function of regulatory T cells was downregulated. Finally, CXCL13 expression was higher in RA synovial fluid than in tonsils, but CCL21 expression was comparable in synovial fluid from all groups and in tonsils. These data demonstrate that increased lymphocyte infiltration in RA synovial fluid is correlated with an increase in LTi-like cells and the elevation of the chemokine expression.

Wnt-C59 inhibits proinflammatory cytokine expression by reducing the interaction between β-catenin and NF-κB in LPS-stimulated epithelial and macrophage cells

  • Jang, Jaewoong;Song, Jaewon;Sim, Inae;Yoon, Yoosik
    • The Korean Journal of Physiology and Pharmacology
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    • v.25 no.4
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    • pp.307-319
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    • 2021
  • Dysregulation of the Wnt pathway causes various diseases including cancer, Parkinson's disease, Alzheimer's disease, schizophrenia, osteoporosis, obesity and chronic kidney diseases. The modulation of dysregulated Wnt pathway is absolutely necessary. In the present study, we evaluated the anti-inflammatory effect and the mechanism of action of Wnt-C59, a Wnt signaling inhibitor, in lipopolysaccharide (LPS)-stimulated epithelial cells and macrophage cells. Wnt-C59 showed a dose-dependent anti-inflammatory effect by suppressing the expression of proinflammatory cytokines including IL6, CCL2, IL1A, IL1B, and TNF in LPS-stimulated cells. The dysregulation of the Wnt/β-catenin pathway in LPS stimulated cells was suppressed by WntC59 treatment. The level of β-catenin, the executor protein of Wnt/β-catenin pathway, was elevated by LPS and suppressed by Wnt-C59. Overexpression of β-catenin rescued the suppressive effect of Wnt-C59 on proinflammatory cytokine expression and nuclear factor-kappa B (NF-κB) activity. We found that the interaction between β-catenin and NF-κB, measured by co-immunoprecipitation assay, was elevated by LPS and suppressed by Wnt-C59 treatment. Both NF-κB activity for its target DNA binding and the reporter activity of NF-κB-responsive promoter showed identical patterns with the interaction between β-catenin and NF-κB. Altogether, our findings suggest that the anti-inflammatory effect of Wnt-C59 is mediated by the reduction of the cellular level of β-catenin and the interaction between β-catenin and NF-κB, which results in the suppressions of the NF-κB activity and proinflammatory cytokine expression.

Bee Venom Within Liposomes Synergistically Inhibit Atopic Dermatitis in Mice

  • Kim, Joan;Song, Ho Sueb
    • Journal of Acupuncture Research
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    • v.39 no.1
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    • pp.40-48
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    • 2022
  • Background: This study was performed to determine the effects of liposome-encapsulated bee venom (BV) treatment of inflammatory factors in atopic dermatitis (AD) compared with BV treatment. Methods: AD was induced by phthalic anhydride in mice and the effects of BV liposomes were measured. Using Leica Application Suite, thickened epidermis and dermis were measured after BV liposome treatment (0.05 and 0.1 ㎍/mL). The number of stained mast cells and the concentration of immunoglobulin (Ig)E were measured. Serum IgE concentration was analyzed using an enzyme-linked immunosorbent assay. The serum concentrations of interleukin (IL)-1, IL-4, and IL-6 inflammatory cytokines were measured. The levels of messenger ribonucleic acid expression of proinflammatory cytokines and chemokines were measured using reverse transcription polymerase chain reaction. Inhibition of mitogen-activated protein kinase activation, was analyzed on western blot. To measure the transcriptional activity (NF-κB inhibition by BV liposomes), western blots (p65, p-IκB, p50, and IκB) were also performed. Results: The weight of lymph nodes, serum IgE concentrations, morphological changes in the skins from the backs of the mice, and mast cell numbers in inflamed tissues were noticeably lower in the BV liposome treatment group compared with the BV treatment group. The concentrations of pro-inflammatory cytokines (IL-1, IL-4, IL-6) and chemokines (TSLP, CCL22) were also reduced. Activation of mitogen-activated protein kinase (p-ERK and p-p38), and transcriptional activity (p65, p-IκB, p50, and IκB) was strongly suppressed in the BV liposome group. Conclusion: BV liposomes may have a better therapeutic effect than BV for the treatment of AD.