• Korean Journal of Plant Resources
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• v.3 no.2
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• pp.83-89
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• 1990

The underground parts of foso rugoso(Rosaceae) , which have been used as an antidiabetic in the folk medicines of Korea, lowered the blood pressure inthe normal rat . And from the chloroform soluble fraction, euscaphic acid wasisolated with $\beta$ -sitosterol and campesterol .

• Proceedings of the PSK Conference
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• 2002.04a
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• pp.117.2-118
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• 2002

• Proceedings of the PSK Conference
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• 2002.04a
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• pp.120.3-121
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• 2002

• Proceedings of the PSK Conference
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• 2002.04a
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• pp.118.1-118.1
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• 2002

• YAKHAK HOEJI
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• v.37 no.3
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• pp.270-277
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• 1993

It is well known that lipidperoxide, formed in vivo, induced the denaturation of enzyme and destruction of cell membrane to acute injury of tissue. Aralia elata have physiological activates, the improvement of lipid metabolism, antidiabetic activity etc., which was thought to have the relationship to lipid peroxidation. The anti-lipidperoxidative effect of Aralia elata have not yet established. In this study, we examined the anti-lipidperoxidative effects of Aralia elata (Butanol fraction) on CCI$_{4}$ induced lipidperoxidation in rats, and elucidated the anti-lipidperoxidative mechanism. In rat liver homogenate intoxicated with CCI$_{4}$ (0.5 ml/100g), BuOH fraction of Aralia elata (80 mg/Kg/day) exhibited 85.41% anti-lipidperoxidative effect but in serum 69.63% inhibitory effects, respectively. In mitochondrial and microsomal fraction showed inhibition of 55.85% and 69.30%, respectively. In order to elucidate the mechanism of anti-lipidperoxidation effects of Aralia elata, enzymatic (NADPH dependent) and non-enzymatic (Ascorbic acid catalyzed) reaction, in vitro, were performed. In enzymatic reation, Aralia elata exhibited 59.43% anti-lipidperoxidation effects, but in non-enzymatic reaction exhibited 43.27% inhibition. Therefore, it is noteworthy that antioxidative power of them may mainly results from the inhibition by enzymatic reaction.

• YAKHAK HOEJI
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• v.42 no.6
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• pp.613-620
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• 1998

Antidiabetic activity of Mori folium ethanol soluble fraction (MFESF) was examined in db/db mice, which is a spontaneously hyperglycemic, hyperinsulinemic and obese animal model . 500 and 1000mg/kg dose for MFFSF (designated by SY 500 and SY 1000, respectively) and 5mg/kg dose for acarbose were administered for 6 weeks. Body weight gain, fasting and non-fasting serum glucose, glycated hemoglobin and triglyceride were all reduced dose dependently when compared between db/db control group and MFESF treated group. At 11th and 13th week after birth, MFESF increased an insulin secretion which may result in lowering serum glucose level. Total activities of sucrase and maltase in SY 500 treated group were decreased when compared to db/db control. On the other hand, those in SY 1000 and acarbose treated groups were increased. This result may suggest that proteins for sucrase and maltase were compensatorily induced due to significant inhibition of glycosidase-catalyzed reaction at doses administered in this study.

• The Korean Journal of Physiology and Pharmacology
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• v.5 no.2
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• pp.183-188
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• 2001

To elucidate antidiabetic effect and mechanism(s) of acarbose in a polygenic spontaneous hyperglycemic and hyperinsulinemic diabetic animal model, $KKA^y$ mice, acarbose was administered orally for 4 weeks and effects on body weight, plasma glucose and insulin levels, genetic expressions of intestinal sucrase-isomaltase (SI), sodium-glucose cotransporter (sGLT1) and glucose transporter in quadriceps muscle (GLUT4) were examined in this study. Although no differences in body weight were detected between control and acarbose-treated groups, plasma glucose level in acarbose-treated group was markedly reduced as compared to the control. In the mechanism study, acarbose downregulated the SI and SGLT1 gene expressions, and upregulated the GLUT4 mRNA and protein expressions when compared to the control group. In conclusion, the data obtained strongly implicate that acarbose can prevent the hyperglycemia in $KKA^y$ mice possibly through blocking intestinal glucose absorption by downregulations of SI and sGLT1 mRNA expressions, and upregulation of skeletal muscle GLUT4 mRNA and protein expressions.

• Bulletin of the Korean Chemical Society
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• v.33 no.11
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• pp.3772-3776
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• 2012

Mitogen-activated protein kinase phosphatase 4 (MKP4) has proved to be a promising target for the development of therapeutics for the treatment of diabetes and the other metabolic diseases. Here, we report an example for a successful application of the structure-based virtual screening to identify three novel inhibitors of MKP4. These inhibitors have desirable physicochemical properties as a drug candidate and reveal a moderate potency with $IC_{50}$ values ranging from 4.9 to $32.3{\mu}M$. Therefore, they deserve consideration for further development by structure-activity relationship studies to optimize the inhibitory and antidiabetic activities. Structural features relevant to the stabilization of the newly identified inhibitors in the active site of MKP4 are discussed in detail.

• Natural Product Sciences
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• v.13 no.4
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• pp.295-299
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• 2007

The methanol extract of seeds of Swietenia macrophylla King. (MESM) was studied for its antidiabetic activity in streptozotocin induced diabetic rats. It was principally aimed to correlate the efficacious role of MESM on reduction of oxidative state associated with diabetes. The extract was found to be potent antidiabetic evidenced by significant reduction of blood glucose level in diabetic rats (47.96% reduction of blood glucose level, at 300 mg/kg, on day 10). It was found that, MESM at 300 mg/kg, significantly decreased TBARS (35.03 and 22.22%) whilst increased GSH (86.75 and 31.45%), SOD (93.05 and 45.88%) and CAT (56.99 and 68.46%) levels in liver and kidney respectively in diabetic rats.

• Journal of Nutrition and Health
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• v.47 no.3
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• pp.167-175
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• 2014

Purpose: Previous studies have shown that treatment with Smilax china L. leaf extract (SCLE) produces antidiabetic effects due to ${\alpha}$-glucosidase inhibition. In this study, we examined the mechanism underlying these antidiabetic effects by examining glucose uptake in HepG2 cells cultured with SCLE. Methods: Glucose uptake and glucokinase activity were examined using an assay kit. Expression of glucose transporter (GLUT)-2, GLUT-4, and HNF-$1{\alpha}$ was measured by RT-PCR or western blot. Results: Treatment with SCLE resulted in enhanced glucose uptake in HepG2 cells, and this effect was especially pronounced when cells were cultured in an insulin-free medium. SCLE induced an increase in expression of GLUT-2 but not GLUT-4. The increase in the levels of HNF-$1{\alpha}$, a GLUT-2 transcription factor, in total protein extract and nuclear fraction suggest that the effects of SCLE may occur at the level of GLUT-2 transcription. In addition, by measuring the change in glucokinase activity following SCLE treatment, we confirmed that SCLE stimulates glucose utilization by direct activation of this enzyme. Conclusion: These results demonstrate that the potential antidiabetic activity of SCLE is due at least in part to stimulation of glucose uptake and an increase in glucokinase activity, and that SCLE-stimulated glucose uptake is mediated through enhancement of GLUT-2 expression by inducing expression of its transcription factor, HNF-$1{\alpha}$.