• Journal of Gastric Cancer
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• v.8 no.3
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• pp.120-128
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• 2008

Purpose: Mistletoe extract was widely used for cancer treatment as complementary or alternative therapy in European area from early twenty century. It is currently used as alternative anti-cancer remedy by piecemeal in domestic medical group, however, the anti-cancer mechanism of mistletoe extract was not known precisely until now. In this study the effect of mistletoe extract on gastric cancer was studied vis cell line experiments. Materials and Methods: The SNU719 gastric cancer cell line was used, and ABNOBAviscum-Q and ABNOBAviscum-F were treated to cells as mistletoe extract, or 5-FU and cisplatin were used with mistletoe extract. The cell viability and cell death rate were estimated by CCK-8 assay kit and lactate dehydrogenase (LDH) assay kit in each. Caspase 3 assay kit was used to measure caspase 3 activity. The protein expression amounts of Bcl2, p53, and PTEN were estimated through Western blot analysis. Results: The co-treatments of mistletoe extract Q/F and 5-FU/cisplatin decreased lesser cell viability than only mistletoe treat. Caspase 3 activity was increased 4~6 times in co-treatment of mistletoe extracts and 5-FU than control. Bcl2 protein expression was reduced by mistletoe extracts or anti-cancer drugs, further more, the co-treatment of mistletoe extracts and 5-FU/cisplatin diminished more the expression than only mistletoe treatment. Mistletoe extracts did not affect the protein expressions of p53 and PTEN. Conclusion: It was concluded that the anti-cancer mechanism of mistletoe extracts was made by caspase 3 activation and lowered Bcl2 expression, and this apoptosis inducing mechanism was independent to p53.

• Journal of The Korean Society of Inherited Metabolic disease
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• v.12 no.2
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• pp.85-93
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• 2012

Purpose: Developmental delay is caused by very diverse etiologic diseases. Most chronic disorders has some influence on development. Chronic or acute disorders of CNS are main etiologic diseases of developmental delay. Up to now, over 60 diseases are included in organic acidopathies and most of them causes acute or chronic recurrent CNS damage and developmental delay. We have done this study to find out the importance of organic acidopathies causing developmental delay in Korean childhood and adolescent patients. Method: Retrograde analysis for 738 patients with developmental delay whose clinical informations are available and have done urine organic acid analysis for 5 years period, between Jan. 1st 2007 to Dec. 31th 2011. Statistical analysis was done with Student's t test using SPSS. Result: Out of 738 patients, 340 patients (46.1%) showed abnormalities on urine organic acid analysis. The most frequent disease was mitochondrial respiratory chain disorders (MRCD) (253, 34.3%), followed by ketolytic defects(39, 5.3%), 3-hydroxyisobutyric aciduria (26, 3.5%), glutaric aciduria type II (8, 1.1%), pyruvate dehydrogenase deficiency (3, 0.4%), 3-methylglutaric aciduria (2, 0.3%), glutaric aciduria type I (2, 0.3%), ethylmalonic aciduria (1, 0.15%), methylmalonic aciduria (1, 0.15%), HMG-CoA lyase deficiency (1, 0.15%), 3-methylcrotonylglycinuria (1, 0.15%), fatty acid oxidation disorders(1, 0.15%) and FAOD (1, 0.15%). Conclusion: Mitochondrial disorders are most frequent etiologic disease on all age group, followed by ketolytic defects and various organic acidopathies. The number and diversities of organic acidopathies emphasize meticulous evaluation of basic routine laboratory examinations and organic acid analysis with initial sample on every developmental patient.

• Journal of Life Science
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• v.26 no.7
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• pp.764-771
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• 2016

Extracts from Artemisia annua Linné (AAE) have been known to possess various functions, including anti-bacterial, anti-virus, and anti-oxidant effects. However, the mechanism of those effects of AAE is not well-known. The aim of this study was to analyze the inhibitory effects of AAE on cell proliferation of the human hepatoma cell line (Hep3B) and to examine its effects on apoptosis. Activation by phosphorylation of Akt is cell proliferation through the phosphorylation of TSC2, mTOR, and GSK-3β. We suggested that AAE may exert cancer cell apoptosis through Akt/mTOR/GSK-3β signal pathways and mitochondria-mediated apoptotic proteins. For this, we examined the effects of extracts of AAE on cell proliferation according to treatment concentration. Treatment with AAE not only reduced cell viability, but also resulted in the induced release of lactate dehydrogenase (LDH). These results were determined with a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and a lactate dehydrogenase (LDH) assay. Furthermore, we determined the effects of apoptosis through Hoechst 33342 staining, annexinⅤ-propidium iodide (PI) staining, 5,5′, 6,6′-tetrachloro-1,1′,3,3′-tetraethyl-imidacarbocyanine iodide (JC-1) staining, and Western blotting. Our study showed that the treatment of liver cancer cells with AAE resulted in the inhibition of Akt, TSC2, GSK-3β-phosphorylated, Bcl-2, and pro-caspase 3 and the activation of Bim, Bax, Bak, and cleaved PARP expressions. These results indicate that AAE induced apoptosis by means of a mitochondrial event through the regulate of Akt/mTOR/GSK-3β signaling pathways.