• Archives of Pharmacal Research
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• v.27 no.7
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• pp.790-796
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• 2004

Ginseng is a shade-loving perennial herb that is cultivated mainly in Korea, Japan, and China. The ginseng root has been used as a tonic remedy, and its antidiabetic activity has been demonstrated as early as 1920s. Although wild ginseng was anecdotally thought to be superior to cultivated ginseng as far as pharmacological properties were concerned, there have been no prior reports on the antidiabetic effect of wild ginseng. In this study, we investigated the preventative anti-diabetic and anti-obese effects of wild ginseng ethanol extract (WGEE). In the preventive experiment, WGEE co-administered with a high fat diet significantly inhibited body weight gain, fasting blood glucose, triglyceride, and free fatty acid levels in a dose dependent manner. WGEE-treated mice at doses of 250 and 500 mg/kg improved the insulin resistance index by 55％ and 61％ compared to the high fat diet (HFD) control, respectively. Diameters of white and brown adipocytes were also decreased by 62％ and 46％ in the WG500-treated group compared to those in HFD fed control mice. Taken together, WGEE has potential as a preventive agent for type 2 diabetes mellitus (and possibly obesity) and deserves clinical trial in the near future.

• Journal of Food Hygiene and Safety
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• v.20 no.1
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• pp.58-63
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• 2005

To assess clastogenic effects of the wild ginseng culture extract (WGCE) in vivo micronucleus test was performed using 7 weeks old ICR mice. At 24 hours after 2nd treatment with wild ginseng culture extract at the doses of 0, 500, 1,000, and 2,000 mg/kg/day by peritoneal route mice were sacrified and marrow cells were prepared for smear slides. As a result of counting the micronucleated polychromatic erythrocyte (MNPCE) of 2,000 polychromatic erythrocyte(PCE), all treatment groups did not show statistically significant increase than negative control group. And there was no clinical sign connected with injection of wild ginseng culture extract. It was concluded that wild ginseng culture extract did not induce micronucleus in the marrow cells of ICR mice.

• Herbal Formula Science
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• v.13 no.1
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• pp.123-143
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• 2005

Objective : This study was carried out to evaluate the liver toxicities of Wild Aconiti Tuber decoction. Methods : The amounts of aconitine in the methanol extract of Wild Aconiti Tuber was measured by HPLC. Safeties was studied by LD50 in mice. Liver toxicities were evaluated histologically and by CBC, blood chemistry after 2 weeks of 0.4g/kg/day clinical dosage oral administrations in rat. Results : 1. The amounts of aconitine in the methanol extract of Wild Aconiti Tuber is $1.697{\pm}0.052mg/g$. But aconitine was not detected in the water decoction of Wild Aconiti Tuber. 2. To evaluate LD50 and safeties of Wild Aconiti Tuber decoction, ICR mice were given high dose of 2, 5, 10g/kg for single time and were observed for 2 weeks. There were no dead animal and abnormal clinical sign and no abnormalities at the autopsy. So, LD50 was admitted to higher than 10g/kg. 3. After 2 weeks of 0.4g/kg/day clinical dosage oral administrations in rat, there was no significant change in the CBC and blood chemistry. 4. In the liver tissues of clinical dosage, mitotic figures, apoptosis and individual cell death were observed, but clear liver toxicities like fatty liver or necrosis were not observed. the liver tissues of high dose in mice, hydropic changes were getting severe as dose grows. Conclusions : According to the results, though aconitine was not detected in the Wild Aconiti Tuber decoction, 0.4g/kg/day 2 weeks p. o (clinical dosage) group showed weak changes in the liver tissues and high dose group showed liver toxicities like hydropic changes.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.4
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• pp.1375-1383
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• 2015

Background: Objective Myocardin-related transcription factor (MRTF)-A is a Rho signaling-responsive co-activator of serum response factor (SRF). The purpose of this study is to investigate the role of MRTF-A and AQP1 (aquaporin 1) in pathological vascular remodeling. Materials and Methods: MRTF-A, AQP1 and neointima expression was detected both in the wire injured femoral arteries of wild-type mice and the atherosclerotic aortic tissues of $ApoE^{-/-}$ mice. Expression of ICAM-1, matrix metallopeptidase 9 (MMP-9) and integrin ${\beta}1$ were also assayed. The intercourse relationship between the molecules were investigated by interfering RNA and inhibitor assay. Results: MRTF-A and AQP1 expression were significantly higher in the wire injured femoral arteries of wild-type mice and in the atherosclerotic aortic tissues of $ApoE^{-/-}$ mice than in healthy control tissues. Both in wire-injured femoral arteries in MRTF-A knockout ($Mkl1^{-/-}$) mice and atherosclerotic lesions in $Mkl1^{-/-}$; $ApoE^{-/-}$ mice, neointima formation were significantly attenuated and the expression of AQP1 were significantly decreased. Expression of ICAM-1, matrix metallopeptidase 9 (MMP-9) and integrin ${\beta}1$, three SRF targets and key regulators of cell migration, and AQP1 in injured arteries was significantly weaker in $Mkl1^{-/-}$ mice than in wild-type mice. In cultured vascular smooth muscle cells (VSMCs), knocking down MRTF-A reduced expression of these genes and significantly impaired cell migration. Underlying the increased MRTF-A expression in dedifferentiated VSMCs were the down-regulation of microRNA-300. Moreover, the MRTF-A inhibitor CCG1423 significantly reduced neointima formation following wire injury in mice. Conclusions: MRTF-A could be a novel therapeutic target for the treatment of vascular diseases.

• Journal of Pharmacopuncture
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• v.9 no.1
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• pp.127-137
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• 2006

Objective : This experiment was conducted to evaluate inhibitory effects against hepatic metastasis by cultivated wild ginseng Herbal Acupuncture. Methods : Colon26-L5 carcinoma cells were injected through hepatic portal vein to induce hepatic metastatic cancer. After treated cultivated wild ginseng Herbal Acupuncture and investigated various kinds of cytokine level using cytokine chip. Results : 1. Mice treated with cultivated wild ginseng Herbal Acupuncture reduced the level of $IL-l{\alpha}$, $IL-{\beta}$, and $TNF-{\alpha}$ compared to the control group. 2. Mice treated with cultivated wild ginseng Herbal Acupuncture was not showed significant change in the level of IL-4, IL-l0, IL-12 and $INF-{\gamma}$ compared to the control group. 3. Observing the level of various kinds of cytokine, cultivated wild ginseng Herbal Acupuncture was suppressed pro-inflammatory cytokine. These findings indicate cultivated wild ginseng Herbal Acupuncture is possible to use the inflammatory disease and futher studies carry out for the explanation of anticancer mechanism.

• YAKHAK HOEJI
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• v.49 no.4
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• pp.284-290
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• 2005

The ginseng root has been used as a tonic remedy, and its antidiabetic activity has been demonstrated as early as 1920s. Although wild ginseng was anecdotally thought to be superior to cultivated ginseng in terms of pharmacological properties, there have been no prior reports on its improvement of metabolic syndrome. In this study, we figured out whether wild ginseng ethanol extract (WGEE) exerted the preventive effects on high fat diet-induced metabolic syndrome as well as treatment effect in ICR mice. In the preventive mode experiment, WGEE at 500 mg/kg significantly inhibited body weight gain $(16\%)$, fasting blood glucose $(37\%)$ and insulin $(37\%)$, triglyceride $(15\%)$, and free fatty acid levels $(32\%)$ when compared to those in high fat diet (HFD) fed control group. WGEE-treated mice at doses of 250 and 500mg/kg improved the insulin resistance index by $55\%\;and\;61\%$ compared to the HFD control group, respectively. In the treatment mode experiment, WGEE also markedly reduced the blood glucose levels (210 mg/dl in control group was lowered to 167 mg/dl).Taken together, WGEE has potential as a preventive and treatment agent for metabolic syndrome and deserves clinical trial in the near future.

• BMB Reports
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• v.40 no.1
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• pp.36-43
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• 2007

In this study, cutaneous role of IL-4 in UVB-induced apoptosis was investigated using transgenic mice with skin-specific expression of IL-4 (IL-4 Tg mice). The transgenic mice did not show any gross clinical abnormalities. However, epidermis was thickened and increased MHC class II positive cells were detected as well as enhanced expression of inflammatory cytokines such as IL-1 and TNF-$\alpha$ in skin. In addition, histological analysis revealed increased infiltration of lymphocytes, acanthosis, hyperkeratosis, and parakeratosis in skin of IL-4 Tg mice. The physiological effect of IL-4 overexpression in skin against environmental stimulus such as UVB was investigated by irradiating wild-type and IL-4 Tg mice with UVB followed by evaluation of apoptosis. The result demonstrated suppressed apoptosis in epidermis of IL-4 Tg mice compared with wild-type mice. To further assess anti-apoptotic function of IL-4 in keratinocytes, stable cell clones were made where IL-4 was constitutively overexpressed and examined for UVB-induced apoptosis. The results showed that apoptosis was remarkably decreased in IL-4 over-expressing cell clones compared with that in mock transfected cells. Collectively, data presented here shows that IL-4 has an inhibitory effect against UVB-induced apoptosis in keratinocytes, suggesting that IL-4 may be an important regulator in cutaneous immunity against UVB.

• Development and Reproduction
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• v.22 no.3
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• pp.263-273
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• 2018

Aquaporin (AQP) 3, a facilitated transporter of water and glycerol, expresses in placenta and fetal membranes, but the detailed localization and function of AQP3 in placenta remain unclear. To elucidate a role of AQP3 in placenta, we defined the expression and cellular localization of AQP3 in placenta and fetal membranes, and investigated the structural and functional differences between wild-type and AQP3 null mice. Gestational sacs were removed during mid-gestational period and amniotic fluid was aspirated for measurements of volume and composition. Fetuses with attached placenta and fetal membranes were weighed and processed for histological assessment. AQP3 strongly expressed in basolateral membrane of visceral yolk sac cells of fetal membrane, the syncytiotrophoblasts of the labyrinthine placenta and fetal nucleated red blood cell membrane. Mice lacking AQP3 did not exhibit a significant defect in differentiation of trophoblast stem cells and normal placentation. However, AQP3 null fetuses were smaller than their control litter mates in spite of a decrease in litter size. The total amniotic fluid volume per gestational sac was reduced, but the amniotic fluid-to-fetal weight ratio was increased in AQP3 null mice compared with wild-type mice. Glycerol, free fatty acid and triglyceride levels in amniotic fluid of AQP3 null mice were significantly reduced, whereas lactate level increased when compared to those of wild-type mice. These results suggest a role for AQP3 in supplying nutrients from yolk sac and maternal blood to developing fetus by facilitating transport of glycerol in addition to water, and its implication for the fetal growth in utero.

• Asian-Australasian Journal of Animal Sciences
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• v.12 no.3
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• pp.331-335
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• 1999

The present study describes the analysis of the multiphasic growth function (MGF) to body weight in laboratory and wild mice. Three genetic groups of laboratory mice (Mus musculus domesticus) designated $CF_{{\sharp}1}$, C3H/HeNCrj and C57BL/6NCrj, and a genetic group of Yonakuni wild mice (Mus musculus molossinus yonakuni, Yk) were used. Mean body weights of each genetic group-sex subclass from birth to 69 days of age taken at 3-day intervals were analyzed by a monophasic, diphasic and triphasic functions for describing growth patterns. A comparison among the three functions of the MGF was based on the goodness-of-fit criteria: residual standard deviation (RSD), adjusted R-square (Adj $R^2$) and Akaike's information criterion (AIC). Result of this study indicated that body weight averaged heavier for males than for females. Among the four genetic groups within both sexes, $CF_{{\sharp}1}$ showed the highest, subsequent followed by C3H/HeNCrj, C57BL/6NCrj and Yk. Comparison among the three functions revealed that the triphasic function was the best fit to growth data, with the lowest RSD, the highest Adj $R^2$ and the lowest AIC, for the four genetic groups. For the triphasic function, RSD within each genetic group-sex subclass was similar for males and females. Adj $R^2$ was 0.999 for all genetic group-sex subclasses. AIC for laboratory mice males and females ranged from -70.48 to 66.50 and from -92.81 to -68.64, respectively; whereas for Yk wild mice males was -74.29 and females -78.42.

• Oncology Letters
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• v.17 no.1
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• pp.379-387
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• 2019

Lymphocyte antigen 6 family member K (LY6K) is upregulated in a number of types of cancer and promotes tumor cell proliferation and metastasis. In addition, LY6K is involved in tamoxifen resistance in breast cancer. However, the in vivo molecular mechanism of LY6K has not yet been investigated. In the present study, transgenic mice overexpressing human LY6K (hLY6K) were generated using the pMAMneo vector, and the effect of LY6K upregulation in vivo was investigated. A total of 4 transgenic mice were generated, and the gene copy number was examined using reverse transcription-quantitative polymerase chain reaction (RT-qPCR). RT-qPCR demonstrated that mRNA of hLY6K was overexpressed in the thymus and spleen of the transgenic mice compared with wild-type mice. Flow cytometric analysis demonstrated that the proportions of B and T cells in the spleen were similar in wild-type and transgenic mice; however, the proportion of thymic mature T cells decreased in the transgenic mice, while there was an increase in the proportion of naïve T cells. These findings suggest that the overexpression of LY6K suppresses T cell development, and that LY6K is a potential therapeutic target for cancer.