• Journal of Ginseng Research
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• 제36권2호
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• pp.153-160
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• 2012

Panax ginseng has long been used as a traditional herbal medicine. More recently, it has received attention for its anti-diabetic and anti-obesity effects in humans and in animal models of type 2 diabetes. In the present study, we tested the hypoglycemic effects of ginseng berry extract in beta-cell-deficient mice and investigated the mechanisms involved. Red (ripe) and green (unripe) berry extracts were prepared and administered orally (100 or 200 mg/kg body weight) to streptozotocin-induced diabetic mice daily for 10 wk. The body weight was measured daily, and the nonfasting blood glucose levels were measured after 5 and 10 wk after administration. Glucose tolerance tests were performed, and the serum insulin levels were measured. The proliferation of beta-cells was measured in vitro. The administration of red or green ginseng berry extract significantly reduced the blood glucose levels and improved the glucose tolerance in beta-cell deficient mice, with the higher doses resulting in better effects. Glucose-stimulated insulin secretion was significantly increased in berry extract-treated mice compared with streptozotocin-induced diabetic control mice. Treatment with ginseng berry extract increased beta-cell proliferation in vitro. Both red berry and green berry extracts improved glycemic control in streptozotocin-induced diabetic mice and increased insulin secretion, possibly due to increased beta-cell proliferation. These results suggest that ginseng berry extracts might have beneficial effects on beta-cell regeneration.

• Advances in Traditional Medicine
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• 제4권1호
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• pp.37-43
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• 2004

The effects of Aegle marmelos (Rutaceae) leaf, Emblica officinalis (Euphorbiaceae) fruit and Ocimum sanctum. (Labiateae) leaf extracts were studied in L-thyroxine (0.5 mg/kg) induced hyperthyroidic mice. Separately combined effects of these three plant extracts and of a commonly used antithyroidic drug, Propyl thiouracil (PTU) were investigated for comparison. Serum concentration of thyroxine $(T_4)$, triiodothyronine $(T_3)$, glucose and the activity of hepatic Glucose 6-Phosphatase (G-6-Pase) were considered as main parameters. Hepatic lipid peroxidation (LPO), superoxide dismutase (SOD) and Catalase (CAT) activities were also studied to reveal the toxic effect of the plant extracts, if any. While exogenous $T_4$ enhanced serum concentration of $T_4$, $T_3$, glucose and the activity of hepatic G-6-Pase, a simultaneous administration of either A. marmelos leaf (1.0 mg/kg), E. officinalis fruit( 30 mg/kg) and O. sanctum leaf (50 mg/kg) extracts, to hyperthyroidic animals decreased all these parameters. However, the effects were more pronounced, as nearly normal thyroid function and serum glucose concentration were exhibited when all three plant extracts were administered together. A decrease in LPO and a concomitant increase in SOD and the CAT activities indicated the safe and antiperoxidative nature of the plant extracts, administered either alone or in combination. Our findings reveal that the three test plant materials exhibit synergistic effects without any hepatotoxicity, suggesting their potential use in the amelioration of hyperthyroidism and/ or hyperglycaemia.

• Clinical and Experimental Reproductive Medicine
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• 제41권1호
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• pp.15-20
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• 2014

Objective: Combined oral contraceptives (COCs) have some adverse effects on the serum lipid profile. Because hyperlipidemia is one of the risk factors in cardiovascular diseases, lipid abnormalities should be evaluated in women consuming COCs. Vitamins E and C are known to have beneficial effects on serum lipid profiles. Therefore, in this study, we evaluated the effects of vitamins E and C on serum lipids in women using COCs. Methods: The study compared changes in lipid parameters with and without vitamin therapy in women consuming COCs compared to those of a control group (40 non-contraceptive users or NCU) for 4 weeks. Total cholesterol and triglyceride, low-density lipoprotein (LDL), and high-density lipoprotein (HDL) levels along with HDL/LDL ratios were measured for all participants. Results: COC users experienced significantly higher increases in the levels of triglycerides and LDL than non-users (p<0.05). However, no significant differences were noted in the total cholesterol and HDL levels. In the treated COC group receiving vitamins E and C, the HDL level and the HDL/LDL ratio increased and the LDL and triglycerides levels decreased significantly compared with those of the other groups. Conclusion: The results of our study indicate that supplementation with antioxidant vitamins E and C restores a normal lipid profile in COC users.

• 건축역사연구
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• 제21권4호
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• pp.93-106
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• 2012

Jean Renaudie was an French architect who designed many urban social housing in France, especially in the city of Ivry-sur-Seine, near Paris, with Renee Gailhoustet, co-responsible as the architect of this city, communist city from long time. He was formed as an architect by the influence of Auguste Perret and Marcel Lods, two french architects, great specialist of the structure of concrete. He formed the Atelier Montrouge with Pierre Riboulet, Gerard Thurnauer, Jean-Louis Verret, and proposed many innovative projects, based on geometrically pure forms and masses. After he joined Renee Gailhoustet, the architect of the City of Ivry-sur-Seine, as a co-responsible for the redevelopment of this ideologically communist city. His urban housing concept approached to take the function as a space to welcome the urban life of the resident, not to offer the physical provision of housing repeating the simple housing unity. He accentuated the social role of Housing project not only as the level of a personal home but also as that of an urbanism. He offered divers choice opportunity to the citizen by the urban functional complex through his efforts to make characteristic complex of urban housing, and by the consequence, the innovative result was done which ameliorated the quality of life for resident. This is an exceptional example, not only in France but even in whole over the world. But the maintenance of building against the oldness and the closing shop of inside commercial zone of Jeanne Hachette became a problem, not only that of physical amelioration but also that of spiritual conservation of the works of Jean Renaudie.

• Korean Journal of Acupuncture
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• 제31권4호
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• pp.234-239
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• 2014

Objectives : The purpose of this study is to report that acupuncture of Damjeonggyeok(tonifying GB in Sa-Am acupucture) can be effective on chronic insomnia. Methods : The patients were treated with Sa-Am acupucture(Damjeonggyeok) added with HT8 and KI6, once a week. Treatments were performed for 20 minutes. The effectiveness was evaluated using total sleep hours and subjective sleep quality based on the Insomnia Severity Index. Result and Conclusions : In all patients, the sleep quality evaluated with the Insomnia Severity Index has shown amelioration and sleeping time was increased. Also, they quit the insomnia pills. Acupuncture at Damjeonggyeok added with HT8 and KI6 seems to be able to one of useful therapies for the sleep disorder in chronic insomnia.

• Molecules and Cells
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• 제38권10호
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• pp.843-850
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• 2015

The1hepatic cell death induced by acetaminophen (APAP) is closely related to cellular adenosine triphosphate (ATP) depletion, which is mainly caused by mitochondrial dysfunction. Adenosine monophosphate (AMP)-activated protein kinase (AMPK) is a key sensor of low energy status. AMPK regulates metabolic homeostasis by stimulating catabolic metabolism and suppressing anabolic pathways to increase cellular energy levels. We found that the decrease in active phosphorylation of AMPK in response to APAP correlates with decreased ATP levels, in vivo. Therefore, we hypothesized that the enhanced production of ATP via AMPK stimulation can lead to amelioration of APAP-induced liver failure. A769662, an allosteric activator of AMPK, produced a strong synergistic effect on AMPK Thr172 phosphorylation with APAP in primary hepatocytes and liver tissue. Interestingly, activation of AMPK by A769662 ameliorated the APAP-induced hepatotoxicity in C57BL/6N mice treated with APAP at a dose of 400 mg/kg intraperitoneally. However, mice treated with APAP alone developed massive centrilobular necrosis, and APAP increased their serum alanine aminotransferase and aspartate aminotransferase levels. Furthermore, A769662 administration prevented the loss of intracellular ATP without interfering with the APAP-mediated reduction of mitochondrial dysfunction. In contrast, inhibition of glycolysis by 2-deoxy-glucose eliminated the beneficial effects of A769662 on APAP-mediated liver injury. In conclusion, A769662 can effectively protect mice against APAP-induced liver injury through ATP synthesis by anaerobic glycolysis. Furthermore, stimulation of AMPK may have potential therapeutic application for APAP overdose.

• Molecules and Cells
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• 제39권4호
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• pp.337-344
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• 2016

Intravenous administration of mesenchymal stem cells (IV-MSC) protects the ischemic rat brain in a stroke model, but the molecular mechanism underlying its therapeutic effect is unclear. We compared genomic profiles using the mRNA microarray technique in a rodent stroke model. Rats were treated with $1{\times}10^6$ IV-MSC or saline (sham group) 2 h after transient middle cerebral artery occlusion (MCAo). mRNA microarray was conducted 72 h after MCAo using brain tissue from normal rats (normal group) and the sham and MSC groups. Predicted pathway analysis was performed in differentially expressed genes (DEGs), and functional tests and immunohistochemistry for inflammation-related proteins were performed. We identified 857 DEGs between the sham and normal groups, with the majority of them (88.7%) upregulated in sham group. Predicted pathway analysis revealed that cerebral ischemia activated 10 signaling pathways mainly related to inflammation and cell cycle. IV-MSC attenuated the numbers of dysregulated genes in cerebral ischemia (118 DEGs between the MSC and normal groups). In addition, a total of 218 transcripts were differentially expressed between the MSC and sham groups, and most of them (175/218 DEGs, 80.2%) were downregulated in the MSC group. IV-MSC reduced the number of Iba-$1^+$ cells in the peri-infarct area, reduced the overall infarct size, and improved functional deficits in MCAo rats. In conclusion, transcriptome analysis revealed that IV-MSC attenuated postischemic genomic alterations in the ischemic brain. Amelioration of dysregulated inflammation- and cell cycle-related gene expression in the host brain is one of the molecular mechanisms of IV-MSC therapy for cerebral ischemia.

• The Korean Journal of Physiology and Pharmacology
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• 제12권1호
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• pp.7-12
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• 2008

OLETF (Otsuka Long-Evans Tokushima Fatty) rats are characterized by obesity-related insulin resistance, which is a phenotype of type 2 diabetes. Sulfonylurea drugs or benzoic acid derivatives as inhibitors of the ATP-sensitive potassium $(K_{ATP})$ channel are commercially available to treat diabetes. The present study compared sulfonylurea drugs (glimepiride and gliclazide) with one of benzoic acid derivatives (repaglinide) in regard to their long-term effect on ameliorating insulin sensitivity in OLETF rats. Each drug was dissolved and fed with drinking water from 29 weeks of age. On high glucose loading at 45 weeks of age, response of blood glucose recovery was the greatest in the group treated with glimepiride. On immunohistochemistry analysis for the Kir6.2 subunit of $K_{ATP}$ channels, insulin receptor ${\beta}$-subunits, and glucose transporters (GLUT) type 2 and 4 in liver, fat and skeletal muscle tissues, the sulfonylurea drugs (glimepiride and gliclazide) were more effective than repaglinide in recovery from their decreased expressions in OLETF rats. From these results, it seems to be plausible that $K_{ATP}$-channel inhibitors containing sulfonylurea moiety may be much more effective in reducing insulin resistance than those with benzoic acid moiety. In contrast to gliclazide, non-tissue selectivity of glimepiride on $K_{ATP}$ channel inhibition may further strengthen an amelioration of insulin sensitivity unless considering other side effects.

• The Plant Pathology Journal
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• 제36권3호
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• pp.218-230
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• 2020

Net blotch of barley caused by Pyrenophora teres (Died.) Drechsler, is one of the most destructive diseases on barley in Algeria. It occurs in two forms: P. teres f. teres and P. teres f. maculata. A total of 212 isolates, obtained from 58 fields sampled in several barley growing areas, were assessed for fungicide sensitivity by target gene analysis. F129L and G137R mitochondrial cytochrome b substitution associated with quinone outside inhibitors (QoIs) resistance, and succinate dehydrogenase inhibitors (SDHIs) related mutations (B-H277, C-N75S, C-G79R, C-H134R, and C-S135R), were analyzed by pyrosequencing. In vitro sensitivity of 45 isolates, towards six fungicides belonging to three chemical groups (QoI, demethylase inhibitor, and SDHI) was tested by microtiter technique. Additionally, sensitivity towards three fungicides (azoxystrobin, fluxapyroxad, and epoxiconazole) was assessed in planta under glasshouse conditions. All tested isolates were QoI-sensitive and SDHI-sensitive, no mutation that confers resistance was identified. EC₅₀ values showed that pyraclostrobin and azoxystrobin are the most efficient fungicides in vitro, whereas fluxapyroxad displayed the best disease inhibition in planta (81% inhibition at 1/9 of the full dose). The EC₅₀ values recorded for each form of net blotch showed no significant difference in efficiency of QoI treatments and propiconazole on each form. However, in the case of fluxapyroxad, epoxiconazole and tebuconazole treatments, analysis showed significant differences in their efficiency. To our knowledge, this study is the first investigation related to mutations associated to QoI and SDHI fungicide resistance in Algerian P. teres population, as well as it is the first evaluation of the sensitivity of P. teres population towards these six fungicides.

• Biomolecules & Therapeutics
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• 제25권3호
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• pp.249-258
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• 2017

To examine the effect of biflorin, a component of Syzygium aromaticum, on memory deficit, we introduced a scopolamine-induced cognitive deficit mouse model. A single administration of biflorin increased latency time in the passive avoidance task, ameliorated alternation behavior in the Y-maze, and increased exploration time in the Morris water maze task, indicating the improvement of cognitive behaviors against cholinergic dysfunction. The biflorin-induced reverse of latency in the scopolamine-treated group was attenuated by MK-801, an NMDA receptor antagonist. Biflorin also enhanced cognitive function in a naïve mouse model. To understand the mechanism of biflorin for memory amelioration, we performed Western blot. Biflorin increased the activation of protein kinase C-${\zeta}$ and its downstream signaling molecules in the hippocampus. These results suggest that biflorin ameliorates drug-induced memory impairment by modulation of protein kinase C-${\zeta}$ signaling in mice, implying that biflorin could function as a possible therapeutic agent for the treatment of cognitive problems.