• 생명과학회지
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• 제20권3호
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• pp.430-436
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• 2010

오미자의 헥산 추출물로부터 dibenzocyclooctadiene류인 schisandrin 1143.7 mg, schisandrin C 317.3 mg, gomisin A 261.4 mg 및 gomisin N 213.4 mg을 순수분리하여 구조를 동정하였다. 각각의 리그난은 $^1H$-NMR, $^{13}C$-NMR 및 GC-MS 스펙트럼으로부터 구조를 동정하였다. 오미자로부터 분리한 schisandrin, schisandrin C, gomisin A 및 gomisin N을 $10^{-5}\;M$, $10^{-6}\;M$ 및 $10^{-7}\;M$로 조정한 용액에 1시간 침지 후 발아율을 비교하였다. Gomisin A의 처리 시 모든 농도에서 발아율이 억제되었고, 농도가 높을수록 발아 억제효과가 높았다. Gomisin N처리 시에는 대조구에 비하여 모든 농도에서 발아율이 높았다. 리그난 처리 48시간 후 발아율은 대조구와 비교한 결과, schisandrin C와 gomisin A는 발아율을 억제하였다. 따라서 오미자로부터 추출한 리그난은 종자발아를 촉진시키는 효과가 있었고, 이차대사산물로서는 많이 함유되어 있으므로 생장조절제로서 이용가능이 있을 것으로 기대한다.

• The Korean Journal of Physiology and Pharmacology
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• 제22권2호
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• pp.203-213
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• 2018

Tumor undergo uncontrolled, excessive proliferation leads to hypoxic microenvironment. To fulfill their demand for nutrient, and oxygen, tumor angiogenesis is required. Endothelial progenitor cells (EPCs) have been known to the main source of angiogenesis because of their potential to differentiation into endothelial cells. Therefore, understanding the mechanism of EPC-mediated angiogenesis in hypoxia is critical for development of cancer therapy. Recently, mitochondrial dynamics has emerged as a critical mechanism for cellular function and differentiation under hypoxic conditions. However, the role of mitochondrial dynamics in hypoxia-induced angiogenesis remains to be elucidated. In this study, we demonstrated that hypoxia-induced mitochondrial fission accelerates EPCs bioactivities. We first investigated the effect of hypoxia on EPC-mediated angiogenesis. Cell migration, invasion, and tube formation was significantly increased under hypoxic conditions; expression of EPC surface markers was unchanged. And mitochondrial fission was induced by hypoxia time-dependent manner. We found that hypoxia-induced mitochondrial fission was triggered by dynamin-related protein Drp1, specifically, phosphorylated DRP1 at Ser637, a suppression marker for mitochondrial fission, was impaired in hypoxia time-dependent manner. To confirm the role of DRP1 in EPC-mediated angiogenesis, we analyzed cell bioactivities using Mdivi-1, a selective DRP1 inhibitor, and DRP1 siRNA. DRP1 silencing or Mdivi-1 treatment dramatically reduced cell migration, invasion, and tube formation in EPCs, but the expression of EPC surface markers was unchanged. In conclusion, we uncovered a novel role of mitochondrial fission in hypoxia-induced angiogenesis. Therefore, we suggest that specific modulation of DRP1-mediated mitochondrial dynamics may be a potential therapeutic strategy in EPC-mediated tumor angiogenesis.