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논문 기본 정보

자료유형
학술저널
저자정보
Min Ju Kim (연세대학교) Jung Hyun Kwak (연세대학교) Seung Han Baek (연세대학교) Hyun Yang Yeo (국립암센터) Ju Hyun Song (연세대학교) Bong Jun Cho (연세대학교) Oh Yoen Kim (연세대학교)
저널정보
한국식품영양과학회 Journal of Food Science and Nutrition Journal of Food Science and Nutrition Vol.15 No.2
발행연도
2010.6
수록면
137 - 142 (6page)

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Previous studies report that organo-sulfur compounds derived from garlic inhibited smooth muscle cell (SMC) proliferation and induced apoptosis of cancer cells. Recently, lipid-soluble compounds such as diallyl sulfides (DAS) and diallyl disulfides (DADS) have been reported to more effectively suppress tumor cell proliferation. However, there were few studies on the suppressive effects of lipid-soluble garlic sulfur compounds on the proliferation and migration of vascular smooth muscle cells (VSMC). Therefore, this study investigated the effect of DAS and DADS on VSMC proliferation/migration induced by oleic acid (OA), a principal fatty acid in circulating triglyceride of blood stream. Assays performed include a tetrazole (MTT) assay, a wound healing assay and a Western blots. VSMC proliferations were enhanced by OA in a dose-dependent manner at concentrations of 10~50 μM and inhibited by DAS and DADS compared to non-treated control. OA-induced proliferations were also attenuated by DAS and DADS. OA-induced cell migrations were 2.5 times higher than non-treated control, and they were significantly attenuated by DAS (32% at 150 μM and 50% at 200 μM) and DADS (40% at 150 μM and 46% at 200 μM). OA-induced cell migration was also attenuated by PD98059 (ERK inhibitor), SB203580 (P38 inhibitor) and particularly by LY204002 (PI3K inhibitor) and SP600125 (JNK2 inhibitor). Additionally, Western blot assays showed that OA-induced JNK1/2-phosphorylation was down-regulated after treatment with DAS and DADS. In conclusion, the findings of our study support the idea that DAS and DADS may have a suppressive effect on the proliferation and migration of OA-induced VSMC and that this effect may be partly associated with PI3K and JNK2 pathways.

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Abstract
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
ACKNOWLEDGMENT
REFERENCES

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UCI(KEPA) : I410-ECN-0101-2010-511-002450003