• Korean Journal of Food Science and Technology
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• v.46 no.1
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• pp.100-107
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• 2014

We evaluated preventive effects of Suaeda japonica (SJ) and Spergularia marina Griseb (SMG) on the insulin resistance in Otsuka Long-Evans Tokushima Fatty (OLETF) rats. The 10-week old OLETF rats were fed diets containing 3% (w/w) SJ and SMG for 18 weeks. Fasting blood glucose levels in SJ and SMG groups, measured using the oral glucose tolerance test, were lower than that of the control rats. The SMG group showed significantly lower levels of insulin, glycated hemoglobin, triglyceride, and total cholesterol than the control group. In addition, these levels were relatively lower in the SJ group than those in the control rats. The SJ and SMG groups had relatively lower protein levels of nuclear factor-kappa B (NF-${\kappa}B$) p65 in adipose tissue and serine phosphorylated insulin receptor substrate 1 (IRS-1) in skeletal muscle than the control group. These results suggest that SJ and SMG prevent insulin resistance and SMG in particular reduces blood triglyceride and total cholesterol levels.

• Microbiology and Biotechnology Letters
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• v.43 no.2
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• pp.112-119
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• 2015

The anti-inflammatory effect of Sargassum coreanum ethanolic extract (SCEE) was investigated using lipopolysaccharide (LPS)-induced inflammatory responses in this study. It was shown that there was no cytotoxicity in the viability of macrophages treated with SCEE when compared to the control. The production of NO was considerably suppressed by SCEE, approximately up to 50% at 100 μg/ml. This significantly decreased levels of IL-6, TNF-α, and IL-1β. In addition, the expression of iNOS, COX-2, NF-κB was suppressed by SCEE treatment. In in vivo testing, the croton oil-induced mouse ear edema was attenuated by SCEE and there were no mortalities in mice administered with 5000 mg/kg body weight of SCEE over a 2 week observation period. From these results, SCEE inhibits the release of LPS-induced pro-inflammatory cytokines and mediators, suggesting that SCEE could be a potential agent for anti-inflammatory therapies.

• Korean Journal of Plant Resources
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• v.31 no.5
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• pp.466-477
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• 2018

In this study, the anti-inflammatory activities of the extracts of different parts of Hovenia dulcis such as leaves, stems, and roots were investigated. Among them, the roots extract (RE) showed the most potent suppressive effect against pro-inflammatory mediators in LPS-stimulated mouse macrophage cells. RE induced dose-dependent reduction of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) and concomitantly reduced the production of NO and $PGE_2$. Additionally, pre-treatment with RE significantly suppressed the production of inflammatory cytokines, such as tumor necrosis $factor-{\alpha}$ ($TNF-{\alpha}$), interleukin $(IL)-1{\beta}$, and IL-6, as well as mRNA levels. Moreover, phosphorylation of mitogen-activated protein kinases (MAPKs) and nuclear translocation of nuclear factor-kappa B (NF-kB) were also strongly attenuated by RE in RAW264.7 cell. Furthermore, RE induced HO-1 expression through nuclear translocation of nuclear factor E2-related factor 2 (Nrf2) and increase HO-1 activity in RAW264.7 macrophages. Therefore, these results indicate that RE strongly inhibits LPS-induced inflammatory responses by blocking NF-kB activation, inhibiting MAPKs phosphorylation, and enhancing HO-1 expression in macrophages, suggesting that RE of H. dulicis and a major component, 27-O-protocatechuoylbetulinic acid could be applied as a valuable natural anti-inflammatory material.

• The Journal of Internal Korean Medicine
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• v.32 no.2
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• pp.301-321
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• 2011

Objectives : The purpose of this investigation was to evaluate the effects of Coptidis chinesis FRANCH. on the alteration of gene expression in a hypoxic model using cultured rat cortical cells. Methods : E18 rat cortical cells were grown in neurobasal medium containing B27 supplement. On 12 DIV, water extract from Coptidis chinesis FRANCH. was added ($20{\mu}g/ml$) to the culture media 4 hrs. On 14 DIV, cells were given hypoxic insult (2% $O_2$/5% $CO_2$, $37^{\circ}C$, 3 hrs), returned to normoxia and cultured for another 24 hrs. Total RNA was extracted from Coptidis chinesis FRANCH. treated and untreated cultures and alterations in the gene expression were analysed by microarray using rat 5K-TwinChips. Results : Effects on some of the genes whose functions were implicated in neural viability were as follows: the expression of apoptosis-related genes such as Clu (Global M = 1.3), of presynaptic inhibition's genes such as Penk-rs (Global M = 1.97), and of innate immuniti's such as Crp (Global M = 1.95), Defensin (Global M = 2.14), and Dnase1l3 (Global M = 1.57) increased. The expression of neurotrophic genes such as S100b (Global M = 1.42), and $NF{\kappa}B$ (Global M = 2.04) increased. Conclusions : Analysing the genes expressed on microarray, shows Coptidis chinesis FRANCH.protects cells by increasing viability and neural nutrition.

• Asian-Australasian Journal of Animal Sciences
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• v.19 no.10
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• pp.1399-1403
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• 2006

A total of 80 cows, including 40 top mastitis resistant and 40 top mastitis susceptible animals as Group I and Group II, were selected from a population of 520 cows based on clinical mastitis occurrence. PCR-SSCP analysis on four fragments within the 5'region and two fragments of Exons 4,15 of bovine lactoferrin (bLF) revealed that four fragments-P1,P4,E4,E15-had polymorphisms which totally included six base mutations, and only two of them had significant differences in allele frequencies between resistant and susceptible groups, P1 (53.7% vs. 70.0%, p<0.05) and P4 (55.0% vs. 68.8%, p<0.05). Further study on these two promising markers combined with the milk performance traits of cows demonstrated that their selection would result in higher fat percentage (p<0.05), lower Somatic Cell Score (SCS) (p<0.05) and Clinical Mastitis Residuals (CMR) (p<0.01) indicating higher mastitis resistance and lower milk yield (p<0.05). The putative transcription factor binding sites in the 5'region were also studied by using MatInspector 7.2.2 software, and two signal pathways regulating the expression of bLF including the NF-${\kappa}B$ pathway and nuclear hormone receptor pathway were predicted.

• The Korean Journal of Food And Nutrition
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• v.31 no.4
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• pp.495-501
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• 2018

Ultraviolet B (UVB) exposure is a risk factor for skin damage resulting in oxidative stress, inflammation, and cell death. The purpose of this study was to investigate the physicochemical properties of Platycodon grandiflorum (PG) to improve its biological activities using a three-step steaming process. We investigated the protective effects of PG and steamed PG extracts on human dermal fibroblasts (HDFs) against UVB radiation-induced oxidative stress and inflammation as well as the underlying mechanisms. The antioxidant potential of the PG extracts was evaluated by measuring the 2,2-diphenyl-1-picrylhydrazyl (DPPH) and 2,2'-azino-bis(3-ethylbenzothiazoline-6-sulphonic acid (ABTS) scavenging activity. ABTS and DPPH were shown by the 0, 30, and 70% ethanol extracts of 2S-PG and 3S-PG ($IC_{50}$, 28~45 and $27{\sim}30{\mu}g/mL$, respectively). Treatment of UVB-irradiated cells with steamed PG ($25{\sim}400{\mu}g/mL$) did not affect their viability. The streamed PG extract suppressed UVB-induced generation of reactive oxygen species (ROS). In addition, streamed PG extract reduced cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) protein expression in UVB-irradiated HDF, regulating nuclear factor $(NF)-{\kappa}B$ expression. These findings suggest that steamed PG extract may be potentially effective against inflammation associated with UVB-induced oxidation stress.

• Food Science and Biotechnology
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• v.16 no.2
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• pp.205-211
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• 2007

This study was designed to investigate the suppressive effect of chlorophyll a on nitric oxide (NO) production and intracellular oxidative stress. In addition, chlorophyll a regulation of nuclear factor (NF) ${\kappa}B$ activation and inducible NO synthase (iNOS) expression were explored as potential mechanisms of NO suppression in a lipopolysaccharide (LPS)-stimulated macrophage cell line. RAW 264.7 murine macrophages were preincubated with various concentrations ($0-10\;{\mu}g/ mL$) of chlorophyll a and stimulated with LPS to induce oxidative stress and inflammatory response. Treatment with chlorophyll a reduced the accumulation of thiobarbituric acid-reactive substances (TBARS), enhancing glutathione level and the activities of antioxidative enzymes including superoxide dismutase, catalase, glutathione peroxidase (GSH-px), and glutathione reductase in LPS-stimulated macrophages compared to LPS-only treated cells. NO production was significantly suppressed in a dose-dependent manner (p<0.05) with an $IC_{50}$ of $12.8\;{\mu}g/mL$. Treatment with chlorophyll a suppressed the levels of iNOS protein and its mRNA expression. The specific DNA binding activities of NFkB on nuclear extracts from chlorophyll a treated cells were significantly suppressed in a dose-dependent manner with an $IC_{50}$ of $10.7\;{\mu}g/mL$. Chlorophyll a ameliorates NO production and iNOS expression through the down-regulation of NFkB activity, which may be mediated by attenuated oxidative stress in RAW 264.7 macrophages.

• IMMUNE NETWORK
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• v.11 no.4
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• pp.216-222
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• 2011

Background: The ligand for CD137 (CD137L; also called 4-1BBL) is mainly expressed on activated APCs such as dendritic cells, B cells and macrophages. Even though CD137L functions as a trigger of the CD137 signaling pathway for T cell activation and expansion, engagement of CD137L can deliver a signal leading to the production of proinflammatory cytokines in macrophages. Methods: We generated cell-permeable TAT-CD137L cytoplasmic domain fusion protein (TAT-CD137Lct) and examined its ability to initiate the CD137L reverse signaling pathway. Results: Treatment of TAT-CD137Lct induced the production of high levels of IL-6 and TNF-${\alpha}$ mRNAs and proteins in peritoneal macrophages. TAT-CD137Lct increased phosphorylation of Erk, p38 MAPK and Jnk, and activated transcription factors C/EBP and CREB. However, TAT-CD137Lct did not visibly affect the degradation of the inhibitor of NF-${\kappa}B$ ($IkB{\alpha}$). We further demonstrated that JNK activation was required for TAT-CD137Lct-induced production of TNF-${\alpha}$, while activation of Erk and p38 MAPK were involved in IL-6 and TNF-${\alpha}$ production. Conclusion: Our results suggest that TATCD137Lct is an effective activator for the CD137L reverse signaling pathway.

• The Journal of Korean Medicine Ophthalmology and Otolaryngology and Dermatology
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• v.35 no.3
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• pp.36-47
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• 2022

Objectives : The purpose of this study was to evaluate the anti-Inflammatory effect of Hwadokdan(HDD) extracted with water. Methods : We pretreated LPS-activated Raw 264.7 cell with HDD and anti-inflammatory effect of HDD is investigated by measuring NO production, relative iNOS, and TNF-α, IL-6, IL-1β, PGE2 productions level, p-IκBα, IκBα, NFκB. Results : HDD reduced NO production and iNOS protein, TNF-α, IL-6 level at concentration of 100㎍/㎖ and 300㎍/㎖ in LPS-activated Raw 264.7 cell significantly. There wasn't a significant cytotoxicity in MTT assay. And HDD reduced IL-1β level at concentration of 300㎍/㎖ in LPS-activated Raw 264.7 cell significantly. HDD reduced p-IκBα and NFκB protein level at concentration of 300㎍/㎖ in LPS-activated Raw 264.7 cell significantly. And HDD enhanced IκBα protein level at concentration of 100㎍/㎖ and 300㎍/㎖ in LPS-activated Raw 264.7 cell significantly. Conclusions : These suggests that HDD can be used as a therapeutic drug for various inflammatory diseases.

• Journal of Veterinary Science
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• v.24 no.1
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• pp.2.1-2.14
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• 2023

Background: Hypothermia is a crucial environmental factor that elevates the risk of cardiovascular disease, but the underlying effect is unclear. Objectives: This study examined the role of cold stress (CS) in cardiac injury and its underlying mechanisms. Methods: In this study, a chronic CS-induced myocardial injury model was used; mice were subjected to chronic CS (4℃) for three hours per day for three weeks. Results: CS could result in myocardial injury by inducing the levels of heat shock proteins 70 (HSP70), enhancing the generation of creatine phosphokinase-isoenzyme (CKMB) and malondialdehyde (MDA), increasing the contents of tumor necrosis factor-α (TNF-α), high mobility group box 1 (HMGB1) interleukin1b (IL-1β), IL-18, IL-6, and triggering the depletion of superoxide dismutase (SOD), catalase (CAT), and glutathione (GSH). Multiple signaling pathways were activated by cold exposure, including pyroptosis-associated NOD-like receptor 3 (NLRP3)-regulated caspase-1-dependent/Gasdermin D (GSDMD), inflammation-related toll-like receptor 4 (TLR4)/myeloid differentiation factor 88 (MyD88)-mediated nuclear factor kappa B (NF-κB), and mitogen-activated protein kinase (MAPK), as well as oxidative stressinvolved thioredoxin-1/thioredoxin-interacting protein (Txnip) signaling pathways, which play a pivotal role in myocardial injury resulting from hypothermia. Conclusions: These findings provide new insights into the increased risk of cardiovascular disease at extremely low temperatures.