• The Journal of Internal Korean Medicine
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• v.33 no.4
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• pp.429-437
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• 2012

Objectives : Obesity is an important cause of diabetes, and lipotoxicity causes insulin resistance. In this study, we investigated the effects of Salvia miltiorrhiza on high fat diet-induced obese type 2 diabetic mouse models. Methods : Diabetes was induced in ICR male mouse (23~25 g) with Surwit's high fat, high sucrose diet. Mice were divided into 4 groups (n=10) of normal, control, Salvia miltiorrhiza, and metformin. After 8 weeks, body weight, OGTT, fructosamine, lipid profile, serum level of adiponectin and leptin, epididymal fat pad, liver weight and epididymal adipocyte size were measured. Results : Salvia miltiorrhiza significantly reduced oral glucose tolerance levels, fructosamine serum level, epididymal fat weight, and epididymal adipocyte size. Salvia miltiorrhiza also increased HDL-cholesterol, adiponectin and leptin serum levels. Conclusions : These results show that Salvia miltiorrhiza improves insulin resistance. Therefore we suggest that Salvia miltiorrhiza would be an effective treatment for obese type 2 diabetic patients.

• Proceedings of the Korean Society of Toxicology Conference
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• 2000.11a
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• pp.31-41
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• 2000

The major issue in the post genome sequencing era is determination of gene expression patterns in variety of biological systems. A microarray system is a powerful technology for analyzing the expression profile of thousands of genes at one experiment. In this study, we constructed cDNA microarray which carries 2,304 cDNAS derived from oligo-capped mouse cDNA library. Using this hand-made microarray we determined gene expression in various biological systems. To determine tissue specific genes, we compared Nine genes were highly-expressed in adult mouse brain compared to kidney, liver, and skeletal muscle. Tissue distribution analysis using DNA microarray extracted 9 genes that were predominantly expressed in the brain. A database search showed that five of the 9 genes, MBP, SC1, HiAT3, S100 protein-beta, and SNAP25, were previously known to be expressed at high level in the brain and in the nervous system. One gene was highly sequence similar to rat S-Rex-s/human NSP-C, suggesting that the gene is a mouse homologue. The remaining three genes did not match to known genes in the GenBank/EMBL database, indicating that these are novel genes highly-expressed in the brain. Our DNA microarray was also used to detect differentiation specific genes, hormone dependent genes, and transcription-factor-induced genes. We conclude that DNA microarray is an excellent tool for identifying differentially expressed genes.

• BMB Reports
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• v.53 no.9
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• pp.466-471
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• 2020

Several humanized mouse models are being used to study humanspecific immune responses and diseases. However, the pivotal needs of fetal tissues for the humanized mice model have been huddled because of the demand for ethical and medical approval. Thus, we have verified the hematopoietic and immunomodulatory function of HepaRG and developed a new and easy humanized mouse model to replace the use of fetal liver tissue. HepaRG co-transplanted Hu-NSG mice significantly increased CD45+ lymphocytes and CD19+ B cells and CD3+ T cells than normal Hu-NSG, suggesting enhanced reconstitution of the human immune system. These results have improved the applicability of humanized mice by developing new models easily accessible.

• Microbiology and Biotechnology Letters
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• v.7 no.2
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• pp.97-102
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• 1979

An actinomycete, AS-568, which produced an inhibitory substance against succinate dehydrogenase of Ehrlich ascites carcinoma and Sarcoma-180 cells of mouse, was isolated. The inhibitory activity was determined by SDI (Succinate Dehydrogenase Inhibition) method. The active substance was specific against carcinoma cells compared to normal cells in mouse; liver, kidney and brain. The inhibitory ratio was about 50％ after one hr treatment at 37$^{\circ}C$ in vitro. Maximal productivity of active substance was recognized by 5 days culture in glucose-asparagine. The active component in cultural liquid was stable in neutral pH range and heat treatment reasonably, add it was recovered from precipitate by ammonium sulfate or non-dialyrable fraction in cellophane membrane as showing the behavior of high molecular substance.

• Asian-Australasian Journal of Animal Sciences
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• v.19 no.8
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• pp.1100-1105
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• 2006

During involution of the mammary gland after the lactation period, the gland undergoes an extensive epithelial cell death. In our previous study, overexpression of an extracellular proteinase inhibitor (Expi) gene accelerated apoptosis of mammary epithelial cells. Here we found that expression of the cathepsin D gene was induced in the Expi-overexpressed apoptotic cells. To understand the role of cathepsin D in apoptosis, we transfected cathepsin D gene into mammary epithelial HC11 cells and established the stable cell lines overexpressing the cathepsin D gene. We found that overexpression of the cathepsin D gene partially induced apoptosis of mammary epithelial cells. Expression patterns of the cathepsin D gene were examined in mouse mammary gland at various reproductive stages. Expression of the cathepsin D gene was increased during involution stages compared to lactation stages, and highest expression levels were shown at involution on day 4. We also examined expression of the cathepsin D gene in various mouse tissues. Mammary gland at involution on day 2 showed highest levels of cathepsin D mRNA of the mouse tissues that we examined. Liver tissues showed high levels of cathepsin D expression. These results demonstrate that cathepsin D may contribute to the apoptotic process of mammary epithelial cells.

• The Journal of Internal Korean Medicine
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• v.36 no.4
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• pp.447-457
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• 2015

Objectives: This study was undertaken to investigate how Cortex Phellodendri affects metabolic functional change in an experimental rat model of obesity.Methods: An obesity model was induced in a C57BL/6 mouse with a high-fat diet. Mice were divided into three groups (n=6) of normal diet, high-fat diet (=control), and high-fat diet with Cortex Phellodendri. After 12 weeks, we measured the three mice groups’ body weight, FBG, FBI, HOMA-IR, OGTT, the weight of epididymal fat and liver, the percentage of ATM, and the gene expression of TNF-α, IL-10, and CD68.Results: Cortex Phellodendri significantly reduced blood glucose and oral glucose tolerance levels. It also reduced ATM numbers and TNF-α and CD68 gene expression and increased IL-10 gene expression.Conclusions: This study suggests that Cortex Phellodendri normalized the blood glucose and reduced the expression of inflammatory markers. However, with respect to other indicators of metabolic function in obesity, there were no significant results.

• The Journal of Korean Medicine
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• v.34 no.1
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• pp.1-14
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• 2013

Objectives: This study was designed to investigate the anti-obesity, anti-diabetic and anti-inflammatory effects of Platycodi radix on obese type 2 diabetes mouse model. Methods: Obese type 2 diabetes mouse model was induced by Surwit's high fat, high sucrose diet for 8 weeks. Models were divided into 4 groups of normal diet (ND, n=10), high fat and high sucrose diet (HFD, n=10), high fat and high sucrose diet with Platycodi radix (PR, n=10), and high fat and high sucrose diet with Metformin (Met, n=10). Body weights were measured every week. After 7 weeks fasting, blood sugar and oral glucose tolerance tests were conducted. After 8 weeks blood samples were taken from mouse hearts and analyzed biochemically. Lipid profile, fructosamine, leptin and weight of epididymal fat pad and liver were measured. Adipose tissue macrophage percentage was analyzed by fluorescence-activated cell sorting (FACS). Results: Compared with the HFD group, body weight, glucose level, fructosamine, weight of epididymal fat pad and adipose tissue macrophage percentage decreased in the PR group. Conclusions: These results suggest that Platycodi Radix has anti-obesity, anti-diabetic, and anti-inflammatory effects on obese type 2 diabetes mouse model.

• Korean Journal of Veterinary Research
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• v.40 no.3
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• pp.611-625
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• 2000

For the improvement of quality control of laboratory mouse, we investigated the environmental condition, histopathological findings and serological test using ELISA to mouse hepatitis virus(MHV), Mycoplasma pulmonis(MP), Clostridium piliforme(TZ) and Sendai virus (HVJ) of ICR, C57BL/6, CBA and C3H/He mice that were supplied from conventional laboratory animal facility. 1. The ammonia concentration of facility was below the recommended concentration, 15ppm, by the KNIH, and the room temperature($21{\sim}23^{\circ}C$) and relative humidity(40~60%) was optimum range recommend by the Ministry of Health and Welfare, respectively. 2. The incidence rate of inapparent disease was 86.6% and the major findings in the liver were vacuolar degeneration with nucleic pleomorphism. The lung was shown the thickening of alveolar wall and interstitial pneumonia with congestion. The kidney and spleen were observed the mild congestion and extramedullary hematopoiesis, respectively. 3. The positive reaction rates against MHV and MP in serological test was 97.9% and 37.5%, respectively but HVJ and TZ were negative. These results suggest that laboratory mice could be infected with MHV and MP under conventional environments. Therefore we recommend to select thoroughly inapparent infected mice and to convert conventional system into SPF facility as soon as possible.

• Archives of Pharmacal Research
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• v.26 no.10
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• pp.861-867
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• 2003

Inhibitory effect of the lectins (KML-C) isolated from Korean mistletoe (KM; Viscum album coloratum) on tumor metastases produced by murine tumor cells (B16-BL6 melanoma, colon 26M3.1 carcinoma and L5178Y-ML25 lymphoma cells) was investigated in syngeneic mice. An intravenous (i.v.) administration of KML-C (20-50 ng/mouse) 2 days before tumor inoculation significantly inhibited lung metastases of both B16-BL6 and colon 26-M3.1 cells. The prophylactic effect of 50 ng/mouse of KML-C on lung metastasis was almost the same with that of 100 $\mu$ g/mouse of KM. Treatment with KML-C 1 day after tumor inoculation induced a significant inhibition of not only the experimental lung metastasis induced by B16-BL6 and colon 26M3.1 cells but also the liver and spleen metastasis of L5178Y-ML25 cells. Furthermore, multiple administration of KML-C given at 3 day-intervals after tumor inoculation led to a significant reduction of lung metastasis and suppression of the growth of B16-BL6 melanoma cells in a spontaneous metastasis model. In an assay for natural killer (NK) cell activity. i.v. administration of KML-C (50 ng/mouse) significantly augmented NK cytotoxicity against Yac-1 tumor cells 2 days after KML-C treatment. In addition, treatment with KML-C (50 ng/mouse) induced tumoricidal activity of peritoneal macrophages against B16-BL6 and 3LL cells. These results suggest that KML-C has an immunomodulating activity to enhance the host defense system against tumors, and that its prophylactic and therapeutic effect on tumor metastasis is associated with the activation of NK cells and macrophages.

• Journal of Veterinary Science
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• v.22 no.3
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• pp.36.1-36.12
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• 2021

Background: Mouse hepatitis virus (MHV) A59 is a highly infectious pathogen and starts in the respiratory tract and progresses to systemic infection in laboratory mice. The complement system is an important part of the host immune response to viral infection. It is not clear the role of the classical complement pathway in MHV infection. Objectives: The purpose of this study was to determine the importance of the classical pathway in coronavirus pathogenesis by comparing C1qa KO mice and wild-type mice. Methods: We generated a C1qa KO mouse using CRISPR/Cas9 technology and compared the susceptibility to MHV A59 infection between C1qa KO and wild-type mice. Histopathological and immunohistochemical changes, viral loads, and chemokine expressions in both mice were measured. Results: MHV A59-infected C1qa KO mice showed severe histopathological changes, such as hepatocellular necrosis and interstitial pneumonia, compared to MHV A59-infected wild-type mice. Virus copy numbers in the olfactory bulb, liver, and lungs of C1qa KO mice were significantly higher than those of wild-type mice. The increase in viral copy numbers in C1qa KO mice was consistent with the histopathologic changes in organs. These results indicate that C1qa deficiency enhances susceptibility to MHV A59 systemic infection in mice. In addition, this enhanced susceptibility effect is associated with dramatic elevations in spleen IFN-γ, MIP-1 α, and MCP-1 in C1qa KO mice. Conclusions: These data suggest that C1qa deficiency enhances susceptibility to MHV A59 systemic infection, and activation of the classical complement pathway may be important for protecting the host against MHV A59 infection.