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논문 기본 정보

자료유형
학술저널
저자정보
Ki-Seok Choi (가천대학교) Heup Song (가천대학교) Eun-Hee Kim (가천대학교) Jae Hyung Choi (가천대학교) Hua Hong (가천대학교) Young-Min Han (가천대학교) Ki Baik Hahm (가천대학교)
저널정보
고려인삼학회 Journal of Ginseng Research Journal of Ginseng Research Vol.36 No.2
발행연도
2012.4
수록면
135 - 145 (11page)

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초록· 키워드

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Previously, we reported that Helicobacter pylori-associated gastritis and gastric cancer are closely associated with increased levels of hydrogen sulfide (H₂S) and that Korean red ginseng significantly reduced the severity of H. pylori-associated gastric diseases by attenuating H₂S generation. Because the incubation of endothelial cells with H₂S has been known to enhance their angiogenic activities, we hypothesized that the amelioration of H₂S-induced gastric inflammation or angiogenesis in human umbilical vascular endothelial cells (HUVECs) might explain the preventive effect of Korean red ginseng on H. pylori-associated carcinogenesis. The expression of inflammatory mediators, angiogenic growth factors, and angiogenic activities in the absence or presence of Korean red ginseng extracts (KRGE) were evaluated in HUVECs stimulated with the H₂S generator sodium hydrogen sulfide (NaHS). KRGE efficiently decreased the expression of cystathionine b-synthase and cystathionine g-lyase, enzymes that are essential for H₂S synthesis. Concomitantly, a significant decrease in the expression of inflammatory mediators, including cyclooxygenase-2 and inducible nitric oxide synthase, and several angiogenic factors, including interleukin (IL)-8, hypoxia inducible factor-1a, vascular endothelial growth factor, IL-6, and matrix metalloproteinases, was observed; all of these factors are normally induced after NaHS. An in vitro angiogenesis assay demonstrated that NaHS significantly increased tube formation in endothelial cells, whereas KRGE pretreatment significantly attenuated tube formation. NaHS activated p38 and Akt, increasing the expression of angiogenic factors and the proliferation of HUVECs, whereas KRGE effectively abrogated this H₂S-activated angiogenesis and the increase in inflammatory mediators in vascular endothelial cells. In conclusion, KRGE was able to mitigate H₂S-induced angiogenesis, implying that antagonistic action against H₂S-induced angiogenesis may be the mechanism underlying the gastric cancer preventive effects of KRGE in H. pylori infection.

목차

INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
ACKNOWLEDGEMENTS
REFERENCES

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