Ultrastructure of mouse thymus was evaluated, following the administration of potassium dichromate and mercuric chloride, the heavy metals of evironmental pollutants. Potassium dichromate (20 mg/kg) or mercuric chloride solutions (10 mg/kg) were subcutanously injected to the mice. Six hours, three days and two weeks after the injections, animals were sacrificed. Thymic tissues were fixed in 2.5% glutaraldehyde-1.5% paraformaldehyde solutions. The procedure was followed by the fixation in 1% osmium tetroxide solutions. Washed and dehydrated tissue-blocks were embedded in the araldite mixture. Ultra-thin sections were stained with uranyl acetate-lead citrate solutions. Results observed were as follows: 1. In electron microscopy, cortical population of thymocytes in the thymus of experimental groups were reduced. especially in the outer cortex. Subcapsular cortices of potassium dichromate treated mice were filled with many epithelial reticular cells, whereas the similar area of mercuric chloride-treated mice exhibited large intercellular spaces. 2. In the thymus of mercuric chloride treated group, large intercellular spaces were formed by shrinkage of epithelial reticular cells, and the space was invaded by numerous cytoplasmic projections of macrophages. Thymocytes nuded out from the shrunken cytoplasm of epithelial reticular cells, presented numerous microvilli. 3. In the thymus of potassium dicromate treated group, many activated macrophages and plasma cells migrated into thymic cortices. 4. In the perivascular spaces of thymic cortices of potassium dichromate- and mercuric chloride-treated mice, activated macrophages. plasma cells, collagen fibrils, and flocculent substance of exudated materials were exhibited. From the above findifgs, it was concluded that potassium dichromate or mercuric chloride could disturb the normal differentiation or 'education' of T cells in the thymic cortex. In turn, these heavy metals may hurt the immunological defense mechanism.
This study evaluated the protective effects of ginseng leaf extract (GLE) against high fat-diet-induced hyperglycemia and hyperlipidemia, and explored the potential mechanism underlying these effects in C57BL/6J mice. The mice were randomly divided into four groups: normal control, high fat diet control (HFD), GLE-treated at 250 mg/kg, and GLE-treated at 500 mg/kg. To induce hyperglycemic and hyperlipidemic states, mice were fed a high fat diet for 6 weeks and then administered GLE once daily for 8 weeks. At the end of the treatment, we examined the effects of GLE on plasma glucose, lipid levels, and the expression of genes related to lipogenesis, lipolysis, and gluconeogenesis. Both GLE groups lowered levels of plasma glucose, insulin, triglycerides, total cholesterol, and non-esterified fatty acids when compared to those in HFD group. Histological analysis revealed significantly fewer lipid droplets in the livers of GLE-treated mice compared with HFD mice. To elucidate the mechanism, Western blots and RT-PCR were performed using liver tissue. Compared with HFD mice, GLE-treated mice showed higher levels of phosphorylation of AMP-activated protein kinase (AMPK) and its substrate, acetyl-CoA carboxylase, but no differences in the expression of lipogenic genes such as sterol regulatory element-binding protein 1a, fatty acid synthase, sterol-CoA desaturase 1 and glycerol-3-phosphate acyltransferase. However, the expression levels of lipolysis and fatty acid uptake genes such as peroxisome proliferator-activated receptor-$\alpha$ and CD36 were increased. In addition, phosphoenolpyruvate carboxykinase gene expression was decreased. These results suggest that GLE ameliorates hyperglycemia and hyperlipidemia by inhibiting gluconeogenesis and stimulating lipolysis, respectively, via AMPK activation.
Objectives: The root and stem of Sinomenium acutum has been used for treatment of arthritis and neuralgia in oriental medicine. To find new substances of the anti-anaphylactic drugs, we studied Sinomenium acutum. Methods: To investigate the effect of this plant, the effect on anaphylactic reaction, plasma histamine level, and tumor necrosis $factor-{\alpha}-(TNF-{\alpha})$ production were measured after the aqueous extract of Sinomenium acutum stem (SSAE) was administrated to mice and rats. Results: The SSAE (0.1 to 1000 mg/kg) dose-dependently inhibited systemic anaphylactic reaction induced by compound 48/80 in mice. Especially, SSAE reduced compound 48/80-induced anaphylactic reaction with 50% at the dose of 1000 mg/kg. SSAE (100 to 1000 mg/kg) also significantly inhibited local anaphylactic reaction activated by anti-dinitrophenyl (DNP) IgE. When mice were pretreated with SSAE at a concentration ranging from 0.1 to 1000 mg/kg, the plasma histamine levels were reduced in a dose-dependent manner. SSAE (1 to 1000 g/ml) dose-dependently inhibited histamine release from the rat peritoneal mast cells (RPMCs) activated by compound 48/80 or anti-DNP IgE. The level of cAMP in RPMCs, when SSAE was added, increased compared with that of a normal control. In addition, SSAE (0.1 g/ml) had a significant inhibitory effect on anti-DNP IgE-induced $TNF-{\alpha}$ production. Conclusions: These results indicate that SSAE inhibits mast cell-mediated anaphylactic reactions and $TNF-{\alpha}$ production from mast cells.
BACKGROUND/OBJECTIVES: In this study, we investigated whether Gelidium amansii extract (GAE) ameliorates obesity in diet-induced obese (DIO) mice. MATERIALS/METHODS: The mice were maintained on a high-fat diet (HD) for 5 weeks to generate the DIO mouse model. And then mice fed HD plus 0.5% (GAE1), 1% (GAE2) or 2% (GAE3) for 8 weeks. RESULTS: After the experimental period, GAE-supplemented groups were significantly lower than the HD group in body weight gain and liver weight. GAE supplemented groups were significantly lower than the HD group in both epididymal and mesenteric adipose tissue mass. The plasma leptin level was significantly higher in the HD group than in GAE-supplemented groups. The leptin level of HD+GAE3 group was significantly lower than that of the HD+conjugated linoleic acid (CLA) group. In contrast, plasma adiponectin level of the HD group was significantly lower than those of HD+GAE2 and HD+GAE3 groups. The expression levels of adipogenic proteins such as fatty acid synthase, sterol regulatory element-binding protein-1c, peroxisome proliferator-activated receptor ${\gamma}$, and CCAAT/enhancer binding protein ${\alpha}$ in the GAE supplemented groups were significantly decreased than those in HD group, respectively. In addition, the expression levels of HD+GAE2 and HD+GAE3 groups are significantly decreased compared to those of HD+CLA group. On the contrary, the expression levels of hormone-sensitive lipase and phospho-AMP-activated protein kinase, proteins associated with lipolysis, were significantly increased in the GAE supplemented groups compared to those in the HD group. HD+GAE3 group showed the highest level among the GAE supplemented groups. CONCLUSIONS: These results suggested that GAE supplementation stimulated the expressions of lipid metabolic factors and reduced weight gain in HD-fed C57BL/6J obese mice.
Having idea to develop more effective anti-diabetic agent from ginseng root, we comprehensively assessed the anti-diabetic activity and mechanisms of ginsam in C57BL/KsJ db/db mice. The db/db mice were divided into 4 groups; diabetic control (DC), ginsam at a dose of 300 or 500 mg/kg (GS300 or GS500) and metformin at a dose of 300 mg/kg (MT300). Ginsam was orally administered for 8 weeks. GS500 reduced the blood glucose concentration and significantly decreased an insulin resistance index. In addition, GS500 reduced the plasma non-esterified fatty acid, triglyceride, and increased high density lipoprotein-cholesterol as well as decreased the hepatic cholesterol and triglyceride. More interestingly, ginsam increased the plasma adiponectin level by 17% compared to diabetic control group. Microarray, quantitative-polymerase chain reaction and enzyme activity results showed that gene and protein expressions associated with glycolysis, gluconeogenesis, and fatty acid oxidation were changed to the way of reducing hepatic glucose production, insulin resistance and enhancing fatty acid $\beta$-oxidation. Ginsam also increased the phosphorylation of AMP-activated protein kinase and glucose transporter expressions in the liver and skeletal muscle, respectively. These changes in gene expression were considered to be the mechanism by which the ginsam exerted the anti-diabetic and anti-dyslipidemic activities in C57BL/KsJ db/db mice.
Plasma cholesterol is increased in normal aging in both rodents and humans. This is associated with reduced elimination of cholesterol and decreased receptor-mediated clearance of plasma low-density lipoprotein (LDL) cholesterol. The aims of this study were: (1) to determine age-related changes in plasma lipid profiles, and (2) to determine the effect of fenofibrate, an activator of peroxisome proliferator activated receptor alpha (PPAR $\alpha$), on plasma lipid profiles in normal rats on a standard diet. Male Sprague-Dawley (SD) rats (n=15) were fed standard chow and water from 10 to 25 weeks of age. During that period, we measured daily food intake, body weight, fasting and random blood glucose levels, plasma total cholesterol (TC), triglycerides (TG), and free fatty acid (FFA) levels. At 20 weeks of age, all rats were randomly divided into two groups: a fenofibrate group (in which rats were gavaged with 300 mg/kg/day of fenofibrate) and a control group (gavaged with water). Fenofibrate treatment lasted 5 weeks. There were no significant changes in daily food intake, blood glucose, and plasma TG level with age. Body weight, plasma TC, and FFA levels were significantly increased with age. Fenofibrate significantly decreased plasma concentrations of TC and FFA, which had been increased with age. However, fenofibrate did not influence the plasma concentration of TG, which had not increased with age. These results suggest that fenofibrate might have a novel role in preventing age-related hypercholesterolemia in SD rats on a normal diet.
The fabrication of Fe alloy-40 wt.%TiC composite materials using spark plasma sintering process after ball-milling was studied. Raw powders to fabricate Fe alloy-TiC composite were Fe alloy, $TiH_{2}$ and activated carbon. Fe alloy powder was Distaloy AE (4%Ni-1%Cu-0.5%Mo-0.01%C-bal.%Fe) made by Hoeganes company with better toughness and lower melting point. These powders were ball-milled in horizontal attrition ball mill at a ball-to-powder weight ratio of 30 : 1. After that, these mixture powders were sintered by using spark plasma sintering apparatus for 5 min at $1200-1275^{\circ}C$ in vacuum atmosphere under $10^{-3}$ torr. DistaloyAE-40 wt.%TiC composite was directly synthesized by dehydrogenation and carburization reaction during sintering process. The phase transformation of as-milled powders and sintered materials was confirmed using X-ray diffraction (XRD) and transmission electron microscope (TEM). The density and harness materials was measured in order to confirm the densification behavior. In case of DistaloyAE-40 wt.%TiC composite retained for 5 min at $1275^{\circ}C$, it has the relative density of about 96% through the influence of rapid densification and fine TiC particle reinforced Fe-based composites materials.
Background: The confirmative diagnosis of pulmonary tuberculosis(Tb) can be made by the isolation of Mycobacterium Tuberculosis(MTb) in the culture of the sputum, respiratory secretions or tissues of the patients, but positive result could not always be obtained in pulmonary Tb cases. Although there are many indirect ways of the diagnosis of Tb, clinicians still experience the difficulty in the diagnosis of Tb because each method has its own limitation. Therefore development of a new diagnostic tool is clinically urgent. It was reported that silica cause some lysosomal enzymes to be released from macrophages in vitro and one of these enzymes is elevated in workers exposed to silica dust and in silicotic subjects. In pulmonary Tb, alveolar macrophages are known to be activated after ingestion of MTb. Activated macrophages can kill MTb through oxygen free radical species and digestive enzymes of lysosome. But if macrophages allow the bacilli to grow intracellularly, the macrophages will die finally and local lesion will enlarge. Then it is assumed that the lysosomal enzymes would be released from the dead macrophages. The goal of this investigation was to determine if there are differences in the plasma activities of lysosomal enzymes, ($\beta$-glucuronidase(GLU) and $\beta$-N-acetyl glucosaminidase(NAG), among the groups of active and inactive pulmonary Tb and healthy control, and to see if there is any possibility that the plasma activity of GLU and NAG can be used as diagnostic indicies of active pulmonary Tb. Methods: The plasma were obtained from 20 patients with bacteriologically proven active pulmonary Tb, 15 persons with inactive Tb and 20 normal controls. In 10 patients with active pulmonary Tb, serial samples after 2 months of anti-Tb medications were obtained. Plasma GLU and NAG activities were measured by the fluorometric methods using 4-methylumbelliferyl substrates. All data are expressed as the mean $\pm$ the standard error of the mean. Results: The activites of GLU and NAG in plasma of the patients with active Tb were $21.52{\pm}3.01$ and $325.4{\pm}23.37$(nmol product/h/ml of plasma), respectively. Those of inactive pulmonary Tb were $24.87{\pm}3.78$, $362.36{\pm}33.92$ and those of healthy control were $25.45{\pm}4.05$, $324.44{\pm}28.66$(nmol product/h/ml of plasma), respectively. There were no significant differences in the plasma activities of both enzymes among 3 groups. The plasma activities of GLU at 2 months after anti-Tb medications were increased($42.18{\pm}5.94$ nmol product/h/ml of plasma) in the patients with active pulmonary Tb compared with that at the diagnosis of Tb(P-value <0.05). Conclusion: The results of the present investigation suggest that the measurement of the plasma activities of GLU and NAG in the patients with active pulmonary Tb could not be a useful method for the diagnosis of active Tb. Further investigation is necessary to define the reasons why the plasma activities of the GLU was increased in the patients with active pulmonary Tb after Tb therapy.
We investigated the long term effects of Sopungsungi-won (SP), a Korean traditional formula used for senile constipation and diabetes mellitus, on the development of diabetic nephropathy (DN) in Zucker diabetic fatty (ZDF) rats. ZDF rats were fed regular laboratory chow mixed with SP or rosiglitazone (RSG) for an 8-week period. Kidney hypertrophy was developed with increasing plasma glucose level, and glomerular hypertrophy was improved by 22% and 45% in SP- and RSG-treated rats, respectively. Urinary glucose and albumin excretions were also significantly lower in SP-treated rats than in ZDF control rats. Activation of the mitogen-activated protein kinase (MAPK)-transforming growth factor ${\beta}1$ (TGF ${\beta}1$)-fibronectin pathway in kidney, responsible for glomerular dysfunction, was markedly blunted by SP treatment in a dose dependent manner. Our findings, for the first time, provide strong evidence that long-term administration of SP formula prevents the development and progression of DN in ZDF rats. Human trials are needed to confirm these experimental results.
Kim, Bang-Hyun;Won, Young-Suk;Kim, Dae-Yong;Kim, Bora;Kim, Eun-Young;Yoon, Mi-Jung;Oh, Goo-Taeg
BMB Reports
/
제42권2호
/
pp.91-95
/
2009
Peroxisome proliferator-activated receptor $\alpha$ and estrogen are believed to be involved in metabolic changes leading to obesity. To test this relationship, we divided female wildtype and PPAR$\alpha$-deficient mice fed on a high fat diet into the following groups: mock-operated, ovariectomized (OVX), and $E_2$-treated. The visceral white adipose tissue and plasma cholesterol levels were increased significantly in wild type OVX and decreased in the $E_2$-treated group, but interestingly not in PPAR$\alpha$-deficient mice. The mRNA levels of lipoprotein lipase in adipose tissue were also increased in only wild type OVX and decreased significantly in $E_2$-treated mice. These novel results suggest the possibility of signaling crosstalk between PPAR$\alpha$ and $E_2$, causing obesity in vivo.
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