• The Journal of Internal Korean Medicine
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• v.26 no.1
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• pp.60-73
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• 2005

Objectives : The aim of this study was to evaluate the effects of Loranthus parasiticus Merr. on cell cycle and expression of related genes in HepG2 cells. Methods : The MTT assay, cell counting assay, $[^3H]-Thymidine$ incorporation assay, flow cytometric analysis, quantitative RT-PCR and western blot assay were studied. Results : In the water extract of Loranthus parasiticus Merr., inhibition of cell proliferation and DNA synthesis in HepG2 cells was seen. These inhibitory effects were due to inhibition of G l-S transition in cell cycle. After treatment with the extract, expression of cyclin D1(G1 check point related gene) was inhibited particularly in dose-dependent and time-dependent manners. Conclusion : These results suggest that the inhibition of cell cycle progression by Loranthus parasiticus Merr. in HepG2 cell is due to suppression of cyclin D1(G1 check point related gene) mRNA expression and protein synthesis.

• Journal of Life Science
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• v.30 no.1
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• pp.18-25
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• 2020

This study was designed to investigate whether Loranthus parasiticus extract (LPE) could inhibit the activities of carbohydrate digestive enzymes and alleviate postprandial hyperglycemia in diabetic mice. Lyophilized L. parasiticus was extracted with 80% ethanol and concentrated. The inhibitory effects of LPE on carbohydrate digestive enzymes were evaluated by examining α-glucosidase and αamylase, and it was seen to inhibit the activities of both enzymes in a dose-dependent manner. More specifically, the IC50 values of LPE against α-glucosidase and α-amylase were 0.121±0.007 and 0.157±0.004 mg/ml, respectively, significantly lower than those of acarbose, showing that LPE has stronger inhibitory effects than the positive control. These results suggest that LPE strongly inhibits the activities of these digestive enzymes. Blood glucose levels in the control group of diabetic mice increased to 490.00±28.52 mg/dl and 474.60±25.30 mg/dl at 60 and 120 min after a meal, respectively. However, when LPE was added to starch, postprandial blood glucose levels were significantly reduced (463.0±23.73 and 418.5±24.50 mg/dl at 60 and 120 min, respectively; p<0.05). The area under the curve also significantly decreased following administration of LPE, with no cytotoxicity. These results therefore indicate that LPE could be used as an α-glucosidase and α-amylase inhibitor and delay carbohydrate digestion and, thus, glucose absorption after a meal.