• Food Science and Biotechnology
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• v.17 no.2
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• pp.336-342
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• 2008

The aim of the present study was to assess the anti-obesity effects of fermented kochujang supplement in C57BL/6J mice. Thirty mice were divided into 3 groups; normal diet control group (ND), high fat diet control group (HD), and high fat diet plus kochujang supplemented group (HDK). Results were as follows: 1. Fennented kochujang supplement in high fat diet decreased body weight and epidydimal and back fat weight compared to non-supplement in HD group. 2. Lipid content and blood glucose level were lower in HDK group than HD group. 3. Fermented kochujang supplement increased mRNA level of lipolytic genes such as acyl-CoA synthetase (ACS), carnitine palmitoyltransferase-1 (CPT-1), and uncoupling proteins-1 (UCP-1) expression, whereas decreased mRNA level of adipogenic genes such as acetyl CoA carboxylase (ACC) expression. These findings suggest that fermented kochujang supplement in high fat diet normalized body weight, epididymal and back fat weight, lipid content, and blood glucose levels through controlling lipid metabolism and provides basic information on the control of obesity.

• The Journal of Internal Korean Medicine
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• v.29 no.3
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• pp.595-607
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• 2008

Objectives: The aim of this study was to determine the effects of Salvia miltiorrhiza (SM) extract in urethane-induced lung tumorigenesis in A/J mice. Methods : We examined change of body weight, histological, apoptosis, immunohistochemical and gene expression of cyclooxygenase (COX-2) in lung tumors. Mice were divided into 3 groups: normal, saline, and experimental group administered SM extract after injection with urethane. Results : Histological observation showed shrunken alveoli in the control group, but recovered from damage in the SM extract administered group. The COX-2 positive materials were observed in the smooth muscle of terminal bronchiole and alveoli from the control group, but these positive materials decreased in the SM extract treatment group. The results of electron microscopical observation, dilated capillary and degenerated endothelia were observed in the control group. The apoptotic nuclei increased more in the control group compared with the normal and SM extract administered groups. Serial sections of the whole lung showed solid and papillary tumors. The size and number of tumors decreased in the SM groups compared with the control groups. Conclusions : These results suggest the possibility that SM may exert an anti-tumor effect on urethane-induced lung tumorigenesis.

• Proceedings of the PSK Conference
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• 2001.04a
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• pp.148.2-149
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• 2001

• Nutrition Research and Practice
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• v.7 no.6
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• pp.446-452
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• 2013

Chronic consumption of a high-fat, high-sucrose (HFHS) diet increases insulin resistance and results in type 2 diabetes mellitus in C57BL/6J mice. Hyperglycemia in diabetics increases oxidative stress, which is associated with a high risk of diabetic complications. The purpose of this study was to examine the hypoglycemic and antioxidant effects of chamnamul [Pimpinella brachycarpa (Kom.) Nakai] in an animal model of type 2 diabetes. The ${\alpha}$-glucosidase inhibitory activity of a 70% ethanol extract of chamnamul was measured in vitro. Five-week-old male C57BL/6J mice were fed a basal or HFHS diet with or without a 70% ethanol extract of chamnamul at a 0.5% level of the diet for 12 weeks after 1 week of adaptation. After sacrifice, serum glucose, insulin, adiponectin, and lipid profiles, and lipid peroxidation of the liver were determined. Homeostasis model assessment for insulin resistance (HOMA-IR) was determined. Chamnamul extract inhibited ${\alpha}$-glucosidase by 26.7%, which was 78.3% the strength of inhibition by acarbose at a concentration of 0.5 mg/mL. Serum glucose, insulin, and cholesterol levels, as well as HOMA-IR values, were significantly lower in the chamnamul group than in the HFHS group. Chamnamul extract significantly decreased the level of thiobarbituric acid reactive substances and increased the activities of superoxide dismutase, catalase, and glutathione peroxidase in the liver compared with the HFHS group. These findings suggest that chamnamul may be useful in prevention of hyperglycemia and reduction of oxidative stress in mice fed a HFHS diet.

• IMMUNE NETWORK
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• v.2 no.3
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• pp.158-165
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• 2002

Background: Toluene diisocyanate (TDI) can cause contact allergy and occupational asthma, but the mechanism underlying sensitization to this chemical compound remains controversal. Also the correlation of mast cell with contact hypersensitivity (CHS) and the role of mast cell in the TDI-induced CHS is unknown. This issue was investigated by administrating TDI on the skin of genetically mast cell-deficient WBB6F1/$J-Kit^{W}/Kit^{W-v}$ ($W/W^{V}$) and congenic normal WBB6F1/J-Kit+/+ (+/+) mice. Methods: To development of animal model of TDI-induced CHS and to investigate the correlation of mast cell with CHS and the role of mast cell in the TDI-induced CHS, $W/W^V$ and +/+ mice were sensitized with TDI on the back skin at day 1 and day 8, and then challenged with 1% TDI on the ear at day 15. At 1, 2, 4, 8, and 24 hours after 1% TDI challenge, the ear thicknesses were measured. It was investigated the histologic changes of dermis in the ear of $W/W^V$ and +/+ mice at 24 hours after 1% TDI challenge. Results: TDI induced a significant ear swelling response in $W/W^V$ and +/+ mice. TDI induced the significant infiltrations of polymorphonuclear leukocytes and eosinophils in $W/W^V$ and +/+ mice, but not of mast cells in normal mice. And TDI increased a characteristic extent of mast cell degranulation in normal mice. There were no significant differences in the ear swelling and the infiltrations of polymorphonuclear leukocytes and eosinophils of normal versus $W/W^V$ mice, either at baseline or after TDI-induced CHS. Conclusion: From the above results, TDI can be used as a murine CHS model, and the mast cells may not be essential in TDI-induced CHS.

• Journal of Microbiology and Biotechnology
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• v.17 no.6
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• pp.1024-1030
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• 2007

We investigated the human apolipoprotein E2 (apoE2) transgenic mouse as an animal model system for age-related macular degeneration (AMD). Transgenic mice expressing human apoE2 and C57BL/6J mice were fed normal chow or a high-fat diet for 4 weeks. Eyes were collected from the mice and lipid deposits in retinal pigment epithelium (RPE) were assessed using electron microscopy. The expressions of apoE, vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), and pigment-epithelium derived factor (PEDF), which are molecular markers for angiogenesis, were assessed with immunohistochemistry. Eyes from apoE2 mice, regardless of diet, contained lipid accumulation in RPE under electron microscopy, whereas control C57BL/6J eyes did not. Lipid accumulation was found predominantly in the RPE and the Bruch's membrane and increased in the eyes of apoE2 mice after one month of a high-fat diet ($8{\pm}2\;per\;50{\mu}m^2$ for normal chow and $11{\pm}2\;per\;50\;{\mu}m^2,\;p<0.05)$. ApoE expression was similar in the apoE2 and control mice; however, VEGF and bFGF were overexpressed in the retinal pigment epithelium of apoE2 eyes compared with control eyes, and PEDF expression was slightly decreased. These expression patterns of VEGF, bFGF, and PEDF suggest angiogenesis is progressing in apoE2 eyes. In conclusion, the eyes of apoE2 mice develop typical lipid accumulations, a common characteristic of AMD, making them a suitable animal model for AMD. The expression profile of VEGF and bFGF on the retinal pigment epithelium suggests that apoE2 may induce neovascularization by altering angiogenic cytokines.

• Asian-Australasian Journal of Animal Sciences
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• v.10 no.4
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• pp.402-407
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• 1997

This study was conducted to investigate the effects of effects of enprostil, a prostaglandin $E_2$, analogue, on liver triacylglycerol content and factors that regulate liver lipid metabolism in mice. Mice received vehicle or $10{\mu}g$ enprostil/kg body weight intraperitoneally every 6 h, and were killed at 0, 6, 12, 18 and 24 h after the first injection. Enprostil significantly lowered liver triacylglycerol content after 12 h of the first injection. However, the peroxisomal ${\beta}$-oxidation activity was inconsistent with the result of liver triacylglycerol content, because its activity was lovered by enprosil. In another experiment, the effect of enprostil on lipid metabolism in mice was investigated in a short period. Mice received $10{\mu}g$ enprostil/kg body weight intraperitoneally, and were killed after 0, 5, 10, 30 and 60 min. After 30 min, malic enzyme activity was significantly increased by the administration of enprostil compared with the activity at 5 min after. No significant changes in liver carnitine palmitoyltransferase and peroxisomal ${\beta}$-oxidation activities were observed. Plasma free fatty acid concentrations were markedly reduced from 5 through 60 min after the administration of enprostil. Consequently, enprostil suppressive effect on liver triacylglycerol concentration might result from the decreased entry of free fatty acid into liver.

• Biomolecules & Therapeutics
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• v.14 no.2
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• pp.106-109
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• 2006

Neprilysin (Nep) is known to be important to degrade $A{\beta}$ derived from amyloid precursor protein (APP) by cleavage with $\beta-and\;\gamma$-secretases. In order to determine whether a correspondence between $A{\beta}-42/{\gamma}-secretase$ activity and Nep levels exists in postnatal aging of transgenic mice expressing either neuron-specific enolase (NSE)-controlled human mutant presenilin-2 (hPS2m) or APPsw alone, the levels of Nep expression and $A{\beta}-42/{\gamma}-secretase$ activity were examined age of 5, 12, and 20 months, respectively. The levels of Nep expression in both types of transgenic brains were decreased relative to those of control mice in a aging-related manner, while the level of $A{\beta}-42/{\gamma}-secretase$ activity was reversibly increased. Thus, changes in $A{\beta}-42$ may all reflect variation in amounts of Nep enzyme.

• Journal of Ginseng Research
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• v.44 no.3
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• pp.519-526
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• 2020

Background: Bisphenol A (BPA), known as an endocrine disruptor, is widely used in the world. BPA is reported to cause inflammation-related diseases. Korean Red Ginseng (KRG) has been used safely in human for a long time for the treatment of diverse diseases. KRG has been reported of its mitigating effect on menopausal symptoms and suppress adipose inflammation. Here, we investigate the protective effect of orally administered KRG on the impacts of BPA in the liver and uterus of menopausal mice model. Methods: The transcriptome analysis for the effects of BPA on mice liver was evaluated by Gene Expression Omnibus (GEO) database-based data (GSE26728). In vivo assay to evaluate the protective effect of KRG on BPA impact in ovariectomized (OVX) mice were designed and analyzed by RNA sequencing. Results: We first demonstrated that BPA induced 12 kinds of gene set in the liver of normal mice. The administration of BPA and KRG did not change body, liver, and uterine weight in OVX mice. KRG downregulated BPA-induced inflammatory response and chemotaxis-related gene expression. Several gene set enrichment analysis (GSEA)-derived inflammatory response genes increased by BPA were inhibited by KRG in OVX mice. Conclusion: Our data suggest that BPA has commonly influenced inflammatory response effects on both normal and OVX mice. KRG protects against BPA impact of inflammatory response and chemotaxis in OVX mouse models. Our comparative analysis will provide new insight into the efficacy of KRG on endocrine disrupting chemicals and OVX mouse.

• Journal of the Korean Society of Food Science and Nutrition
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• v.42 no.8
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• pp.1183-1189
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• 2013

We investigated the effects of oyster shell extract (OSE) on papain-induced osteoarthritis in C57BL/6J mice. Osteoarthritis was induced in mice by a papain injection into the knee joint. The mice were divided into a total of five groups (n=8). The normal group was untreated, whereas the papain group (negative control) was induced with osteoarthritis and treated with water daily. The papain+DS group (positive control) was treated with diclofenac sodium. Papain+OSE groups were treated with OSE concentrations of 100 and 200 mg/kg/bw for 20 days. Proteoglycan content in articular cartilage was analyzed through safranine-O fast green staining and H&E staining. The histopathological changes in cartilage were measured by the Rudolphi score approach. The contents of tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$), interleukin (IL)-$1{\beta}$, and IL-6 in plasma were analyzed by the ELISA method. After experiments, body weights of the treated groups were not significantly different compared with the normal group. Cartilage loss and joint instability significantly improved in a dose-dependent manner in the OSE-treated group compared with the papain group (P<0.05). Proteoglycan content was significantly higher in the OSE-treated group than the papain group (P<0.05). Osteoarthritis scores of the OSE-treated group were significantly decreased compared with the papain group (P<0.05). TNF-${\alpha}$, IL-$1{\beta}$, and IL-6 content in the plasma of the papain+OSE treated groups significantly decreased in a dose-dependent manner compared with the papain group (P<0.05). These results suggest that OSE treatment might have anti-arthritic effects on papain-induced osteoarthritis in C57BL/6J mice.