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ginsenoside rd/hypoxia
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4 結果
Increased ubiquitination of multidrug resistance 1 by ginsenoside Rd.
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MCF-7/ADR cells, a doxorubicin-resistant human breast cancer cell line, acquires resistance to several chemotherapeutic agents, such as anthracylines and taxol, via overexpression of the multidrug resistance1 (MDR1) gene. The present study was designed to clarify whether ginsenosides affect the
Screening of anti-hypoxia/reoxygenation agents by an in vitro model. Part 1: Natural inhibitors for protein tyrosine kinase activated by hypoxia/reoxygenation in cultured human umbilical vein endothelial cells.
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Protein tyrosine kinase (PTK) signaling pathways play important roles in ischemia/reperfusion (I/R) or hypoxia/reoxygenation (H/R) injuries. Inhibition of PTK activation can protect against I/R- or H/R-induced damages. As one part of our work for seeking bioactive compounds from natural sources
A study of ginsenoside-Rd in a renal ischemia-reperfusion model.
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The effect of ginsenoside-Rd in ischemic-reperfused rats was examined. In control rats, blood and renal parameters and the activities of antioxidative enzymes in renal tissue deviated from the normal range, indicating dysfunction of the kidneys. In contrast, when ginsenoside-Rd was given orally for
Screening of anti-hypoxia/reoxygenation agents by an in vitro method. Part 2: Inhibition of tyrosine kinase activation prevented hypoxia/reoxygenation-induced injury in endothelial gap junctional intercellular communication.
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In this study, we demonstrated that hypoxia/reoxygenation (H/R) induced an injury in gap junctional intercellular communication (GJIC) after 2 h of reoxygenation in cultured HUVEC. Free radical scavenger (DMSO) and antioxidant (SOD) did not prevent this GJIC injury at all. Protein kinase C inhibitor
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