• Journal of Life Science
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• v.17 no.1 s.81
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• pp.56-63
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• 2007

Insulin stimulates the fusion of intracellular vesicles containing glucose transporter 4 (GLUT4) with plasma membrane in adipocytes and muscle cells. Here we show that adipocyte differentiation results in enhanced insulin sensitivity of glucose uptake. On the other hand, glucose uptake in response to platelet-derived growth factor (PDGF) stimulation was markedly reduced by adipocyte differentiation. Expression level of insulin receptor and caveolin-1 was dramatically increased during adipocyte differentiation. Adipocyte differentiation caused :ilightly enhanced activation of acutely transforming retrovirus AKT8 in rodent T cell lymphoma (Akt) by insulin stimulation. However, activation of Akt by PDGF stimulation was largely reduced. Activation of ERK was not detected in both fibroblasts and adipocytes after stimulation with insulin. PDGF-dependent activation of ERK was reduced by adipocyte differentiation. Insulin-dependent glucose uptake was abrogated by LY294002, a phosphatidylinositol 3-kinase (PI3K) inhibitor, in both fibroblasts and adipocytes. Also disassembly of caveolae structure by $methyl-\beta-cyclodextrin$ caused impairment of Akt activation and glucose uptake. Finally, insulin receptor, Akt, SH2-domain-containing inositol 5-phosphatase 2 (SHIP2), and regulatory subunit of PI3K are localized at lipid raft domain and the translocation was facilitated upon insulin stimulation. Given these results, we suggest that lipid raft provide proper site for insulin action for glucose uptake.

• Journal of Life Science
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• v.20 no.3
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• pp.388-395
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• 2010

Cyclooxygenase (COX)-2 is generally known as an inducible enzyme, and it produces arachidonic acid to prostaglandin $E_2$ ($PGE_2$), which has been demonstrated to play a critical role in inflammation. In the present study, we investigated the effects of the extracts of fermented beans including soybean (FS), black agabean (FBA) and yellow agabean (FYA), on the expression of COXs and production of $PGE_2$ in U937 human promonocytic cells. Treatment of phorbol 12-myristate 13-acetate (PMA) significantly induced pro-inflammatory mediators such as COX-2 expression and $PGE_2$ production, whereas the levels of COX-1 remained unchanged. However, pre-treatment with FS, FBA and FYA significantly decreased PMA-induced COX-2 protein as well as mRNA, which is associated with inhibition of $PGE_2$ production. Moreover, FS, FBA and FYA markedly prevented the increase of nuclear translocation of nuclear factor kappa B (NF-${\kappa}B$) p65 by PMA. Our data indicate that the extracts of fermented beans exhibits anti-inflammatory properties by suppressing the transcription of pro-inflammatory cytokine genes through the NF-${\kappa}B$ signaling pathway.

• Journal of Life Science
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• v.18 no.3
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• pp.336-343
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• 2008

Histone deacetylases (HDACs) inhibitors have emerged as the accessory therapeutic agents for various human cancers, since they can block the activity of specific HDACs, restore the expression of some tumor suppressor genes and induce cell differentiation, cell cycle arrest and apoptosis in vitro and in vivo. In the present study, we investigated that the effect of trichostatin A (TSA), an HDAC inhibitor, on the cell growth and apoptosis, and its effect on the nuclear factor-kappaB $(NF-{\kappa}B)$ activity in 267B1 human prostate epithelial cells. Exposure of 267B1 cells to TSA resulted in growth inhibition and apoptosis induction in and dose-dependent manners as measured by fluorescence microscopy, agarose gel electrophoresis and flow cytometry analysis. TSA treatment inhibited the levels of IAP family members such as c-IAP-1 and c-IAP-2 and induced the proteolytic activation of caspase-3, -8 and -9, which were associated with concomitant degradation of poly (ADP-ribose)-polymerase, ${\beta}-catenin$ and laminin B proteins. The increase in apoptosis by TSA was connected with the translocation of $NF-{\kappa}B$ from cytosol to nucleus, increase of the DNA binding as well as promoter activity of $NF-{\kappa}B$, and degradation of cytosolic inhibitor of KappaB $(I{\kappa}B)-{\alpha}$ protein. We therefore concluded that TSA demonstrated anti-proliferative and apoptosis-inducing effects on 267B1 cells in vitro, and that the activation of caspases and $NF-{\kappa}B$ may play important roles in its mechanism of action. Although further studies are needed, these findings provided important insights into the possible molecular mechanisms of the anti-cancer activity of TSA.

• The Korean Journal of Food And Nutrition
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• v.28 no.4
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• pp.551-557
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• 2015

The genus Rosa (Rosaceae) is an abundant source of phenolics and is traditionally used as a food supplement and as herbal medicine. Various plant phenolics are known to have anticancer, antioxidant, and anti-inflammatory properties. In this study, we investigated the anti-inflammatory effects of rose methanolic extracts (RMEs) from four different rose cultivars (Macarena, Onnuri, Oklahoma, and Colorado) in lipopolysaccharide (LPS)-activated RAW 264.7 cells. Our results demonstrated that pretreatment of REMs ($500{\mu}g/mL$) significantly reduced NO production by suppressing iNOS protein expression in LPS-stimulated cells. Anti-inflammatory effects by RMEs were observed in the following order: Oklahoma > Colorado > Onnuri > Macarena. Consistent with this finding, RMEs inhibited the translocation of $NF-{\kappa}B$ from the cytosol to the nucleus via the suppression of $I{\kappa}B{\alpha}$ phosphorylation and also inhibited LPS-stimulated $NF-{\kappa}B$ transcriptional activity. These findings suggest that RMEs exert anti-inflammatory actions and help to elucidate the mechanisms underlying the potential therapeutic values of RMEs. Therefore, RMEs could be regarded as a potential source of natural anti-inflammatory agents.

• The Korean Journal of Physiology and Pharmacology
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• v.19 no.5
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• pp.451-460
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• 2015

Sirtuin 1 (SIRT1) is a mammalian $NAD^+$-dependent protein deacetylase that regulates cellular metabolism and inflammatory response. The organ-specific deletion of SIRT1 induces local inflammation and insulin resistance in dietary and genetic obesity. Macrophage-mediated inflammation contributes to insulin resistance and metabolic syndrome, however, the macrophage-specific SIRT1 function in the context of obesity is largely unknown. C57/BL6 wild type (WT) or myeloid-specific SIRT1 knockout (KO) mice were fed a high-fat diet (HFD) or normal diet (ND) for 12 weeks. Metabolic parameters and markers of hepatic steatosis and inflammation in liver were compared in WT and KO mice. SIRT1 deletion enhanced HFD-induced changes on body and liver weight gain, and increased glucose and insulin resistance. In liver, SIRT1 deletion increased the acetylation, and enhanced HFD-induced nuclear translocation of nuclear factor kappa B (NF-${\kappa}B$), hepatic inflammation and macrophage infiltration. HFD-fed KO mice showed severe hepatic steatosis by activating lipogenic pathway through sterol regulatory element-binding protein 1 (SREBP-1), and hepatic fibrogenesis, as indicated by induction of connective tissue growth factor (CTGF), alpha-smooth muscle actin (${\alpha}$-SMA), and collagen secretion. Myeloid-specific deletion of SIRT1 stimulates obesity-induced inflammation and increases the risk of hepatic fibrosis. Targeted induction of macrophage SIRT1 may be a good therapy for alleviating inflammation-associated metabolic syndrome.

• Journal of Microbiology and Biotechnology
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• v.30 no.11
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• pp.1614-1625
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• 2020

A number of species of the genus Trichilia (Meliaceae) exhibit anti-inflammatory effects. However, the effect of Trichilia martiana C. DC. (TM) on lipopolysaccharide (LPS)-induced inflammation has not, to the best of our knowledge, yet been determined. Therefore, in the present study, the antiinflammatory effect of TM on LPS-stimulated RAW264.7 macrophages was evaluated. The ethanol extract of TM (TMEE) significantly inhibited LPS-induced nitric oxide (NO), prostaglandin 2 (PGE₂), inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2). TMEE also reduced the levels of inflammatory cytokines, including tumor necrosis factor-alpha (TNF-α), interleukin (IL)-1β and IL-6. The upregulation of mitogen-activated protein kinases (MAPKs) and NF-κB activation was revealed to be downregulated following TMEE pretreatment. Furthermore, TMEE was indicated to lead to the nucleus translocation of nuclear factor erythroid-derived 2-related factor 2 (Nrf2) and the expression of heme oxygenase-1 (HO-1). In H292 airway epithelial cells, the pretreatment of TMEE significantly downregulated the production of LPS-stimulated IL-1β, and TMEE was indicated to increase the expression of HO-1. In animal models exhibiting LPS-induced acute lung injury (ALI), treatment with TMEE reduced the levels of macrophages influx and TNF-α production in the bronchoalveolar lavage fluid (BALF) of ALI mice. Additionally, TMEE significantly downregulated the activation of ERK, JNK and IκB, and upregulated the expression of HO-1 in the lungs of ALI mice. In conclusion, the results of the current study demonstrated that TMEE could exert a regulatory role in the prevention or treatment of the endotoxin-mediated inflammatory response.

• Journal of Korean Society of Forest Science
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• v.90 no.5
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• pp.600-607
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• 2001

This study was conducted to estimate the capability of Populus alba ${\times}$ glandulosa and Betula schmidtii for the uptake of Pb from the lead-contaminated soil and their tolerance to lead. Rooted cuttings in the former species and germinated seedlings in the latter species were planted in pots and irrigated with Pb-containing water for 60 days. In both tree species, growth inhibition was observed in 800, and 1,500ppm of $Pb(NO_3)_2$. Most Pb was accumulated in plant roots and only a small portion was transported to the shoots. The translocation rates of Pb for B. schmidtii and P. alba ${\times}$ glandulosa were 1.6-2.6% and 1.2-1.6%, respectively. The maximum Pb content accumulated in shoots was 468.0mg/kg d.w. in P. alba ${\times}$ glandulosa, and 602.0mg/kg d.w. in B. schmidtii. Although tolerance to lead was generally higher in B. schmidtii than P. alba ${\times}$ glandulosa, the highest tolerance to lead was observed in P. alba ${\times}$ glandulosa clone, 72-16. Finally, we discussed the applicability of P. alba ${\times}$ glandulosa and B. schmidtii for phytoextraction based on their Pb uptake ability, high biomass production, and easiness in large-scale cultivation.

• The Journal of the Convergence on Culture Technology
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• v.6 no.2
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• pp.543-551
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• 2020

Red rose petals are usually disposed but they are an abundant source of phenolics and traditionally used as food supplement and as herbal medicine. Of the Various phenolics, they are known to have anticancer, antioxidant, and anti-inflammatory properties. In this study, we investigated the anti-inflammatory effects of red rose ethanolic extracts(GRP) on lipopolysaccharide (LPS)-activated RAW 264.7 cells. The results demonstrated that pretreatment of GRP(500㎍/mL) significantly reduced NO production by suppressing iNOS protein expression in LPS-stimulated cells. Anti-inflammatory effects byred rose petal were observed in the following. Red rose petal inhibited the translocation of NF-κB from the cytosol to the nucleus via the suppression of IκB-α phosphorylation and also inhibited LPS-stimulated NF-κB transcriptional activity. These findings suggest that red rose petal exert anti-inflammatory actions and help to elucidate the mechanisms underlying the potential therapeutic values of red rose petal. Therefore, red rose petal could be regarded as a potential source of natural anti-inflammatory agents.

• IMMUNE NETWORK
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• v.11 no.2
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• pp.107-113
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• 2011

Background: Metabolic disorders, including type II diabetes and obesity, present major health risks in industrialized countries. AMP-activated protein kinase (AMPK) has become the focus of a great deal of attention as a novel therapeutic target for the treatment of metabolic syndromes. In this study, we evaluated whether dietary aloe could reduce obesity-induced inflammation and adipogenesis. Methods: Male C57BL/6 obese mice fed a high-fat diet for 54 days received a supplement of aloe formula (PAG, ALS, Aloe QDM, and Aloe QDM complex) or pioglitazone (PGZ) and were compared with unsupplemented controls (high-fat diet; HFD) or mice fed a regular diet (RD). RT-PCR and western blot analysis were used to quantify the expression of obesity-induced inflammation. Results: Aloe QDM complex downregulated fat size through suppressed expression of scavenger receptors on adipose tissue macrophages (ATMs) compared with HFD. Both white adipose tissue (WATs) and muscle exhibited increased AMPK activation through aloe supplementation, and in particular, the Aloe QDM complex. Obesity-induced inflammatory cytokines (IL-$1{\beta}$ and -6) and $HIF1{\alpha}$ mRNA and protein were decreased markedly, as was macrophage infiltration by the Aloe QDM complex. Further, the Aloe QDM complex decreased the translocation of NF-${\kappa}B$ p65 from the cytosol in the WAT. Conclusion: Dietary aloe formula reduced obesity-induced inflammatory responses by activation of AMPK in muscle and suppression of proinflammatory cytokines in the WAT. Additionally, the expression of scavenger receptors in the ATM and activation of AMPK in WAT led to reduction in the percent of body fat. Thus, we suggest that the effect of the Aloe QDM complex in the WAT and muscle are related to activation of AMPK and its use as a nutritional intervention against T2D and obesity-related inflammation.

• Journal of the Korean Society of Food Science and Nutrition
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• v.46 no.4
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• pp.409-416
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• 2017

1,2,3,4,6-Penta-O-galloyl-${\beta}$-D-glucose (PGG) is a gallotannin isolated from Galla Rhois. In a previous study, PGG was shown to suppress the allergic response by attenuating immunoglobulin E production both in vitro and in vivo. However, the effect of PGG on bacteria-induced inflammation at physiological concentration remains unclear. Therefore, the aim of this study was to investigate the effect of PGG on lipopolysaccharide (LPS)-stimulated macrophages. PGG inhibited release of nitric oxide (NO) and prostaglandin $E_2$ by alleviating protein expression of inducible NO synthase and cyclooxygenase-2 in LPS-treated RAW264.7 cells. Furthermore, PGG suppressed the release of interleukin-6 and tumor necrosis factor-${\alpha}$ induced by LPS. Further study indicated that PGG blocked translocation of the p65 subunit of nuclear factor-${\kappa}B$ from the cytosol into the nucleus, which is one of the underlying mechanisms of the anti-inflammatory action of PGG. Collectively, these data suggest that PGG might be useful for the treatment of inflammatory disease.