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Urine metabonomic study for blood-replenishing mechanism of Angelica sinensis in a blood-deficient mouse model 被引量:11
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作者 WANG Tao SUN Hong-Guo +2 位作者 HUA Yong-Li LI Peng-Ling WEI Yan-Ming 《Chinese Journal of Natural Medicines》 SCIE CAS CSCD 2016年第3期210-219,共10页
This study aimed at determining the effects of Angelica sinensis(AS) on urinary metabolites in blood deficiency mice and exploring its replenishing blood mechanism. Gas chromatography–mass spectrometry(GC-MS) was app... This study aimed at determining the effects of Angelica sinensis(AS) on urinary metabolites in blood deficiency mice and exploring its replenishing blood mechanism. Gas chromatography–mass spectrometry(GC-MS) was applied to detect metabolites in the urine samples in different collection periods. Principal component analysis(PCA) and orthogonal partial least squares discriminant analysis(OPLS-DA) were used to investigate the differences in metabolic profiles among control group(CG), blood deficiency model group(MG), AS groups, and Colla Corii Asini group(CCAG). The potential biomarkers were identified based on the variable importance in the projection(VIP), T-test, and National Institute of Standards and Technology(NIST) and mass spectra library. The metabolites were analyzed using metabolomics pathway analysis(Met PA) to build the metabolic pathways. Our results indicated that, on the seventh day, the levels of glucose, lactic acid, pyruvic acid, alanine, acetoacetic acid, and citric acid changed significantly in blood deficiency mice. However, these metabolic deviations came to closer to normal levels after AS intervention. The reversing blood-deficiency mechanism of AS might involve regulating synthesis and degradation of ketone bodies, Pyruvate metabolism, TCA cycle, and Glycolysis / Gluconeogenesis. In conclusion, metabonomics is a robust and promising means for the identification of biomarkers and elucidation of the mechanisms of a disease, thereby highlighting its importance in drug discovery. 展开更多
关键词 Angelica sinensis METABONOMICS GC-MS blood deficiency resistant
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Induction of resistance vessel dilation by ginger root juice,possibly through extracellular signal-regulated kinase 1/2 and endothelial nitric oxide synthase activation in endothelial cells
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作者 Elizabeth Bird Dinesh M.Shah 《Family Medicine and Community Health》 2013年第3期12-18,共7页
Objective:To investigate the effects of ginger root juice on contractibility of resistance blood vessels from mice and on activation of extracellular signal-regulated kinase 1/2(ERK1/2)and endothelial nitric oxide syn... Objective:To investigate the effects of ginger root juice on contractibility of resistance blood vessels from mice and on activation of extracellular signal-regulated kinase 1/2(ERK1/2)and endothelial nitric oxide synthase(eNOS)in human endothelial cells.Methods:Juice was prepared from semi-dry ginger roots.Mesenteric artery rings were dis-sected from healthy adult C57BL/J6 mice.Primary human umbilical vein endothelial cells(HU-VECs)were isolated from umbilical cords of normal full-term babies.The contractibility of the dissected vessel rings in the presence or absence of ginger root juice at 0.1%(v/v)after potassium(100 mM KCL)stimulation was measured by wire myography.The phosphorylation levels of ERK1/2 and eNOS in the presence of ginger root juice in the culture medium at 0,0.025%,0.05%,0.1%,and 0.2%(v/v)in HUVECs were assessed by western blotting analysis.Results:An immediate sharp increase in the contractile activity was observed in mesenteric artery rings in response to KCL stimulation.Ginger root juice effectively attenuated the KCL-mediated vessel contraction.Moreover,ginger root juice significantly increased phosphorylation of ERK1/2 and eNOS in a dose-dependent manner.Conclusions:Ginger root juice is capable of relaxing resistance blood vessels.Activation of ERK1/2 and eNOS through phosphorylation in endothelial cells may be a mechanism underlying the vasodilator activity of ginger root. 展开更多
关键词 GINGER resistance blood vessels VASODILATION ERK1/2 eNOS Phosphorylation MYOGRAPHY Endothelial cell
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