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柱前衍生-RP-HPLC法测定青蒿中青蒿素的含量 总被引:17,自引:0,他引:17
采用柱前衍生-RP-HPLC法测定10个不同产地的青蒿药材中青蒿素的含量.采用Lichrospher 100 RP-18e(250 mm×4.6 mm,5μm,Merck KgaA,Germany)色谱柱,甲醇-0.01 mol/L醋酸钠-醋酸缓冲液(pH 5.8)(体积比62:38)为流动相;检测波长:260 nm;流速:0.5 mL/min;柱温:25℃.结果表明该法准确重现性好,可以为青蒿质量标准的制订提供科学依据. 相似文献
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本文对北京西山海拔300米的26年生人工栓皮栎林的生物量作了测定。粮据十株伐倒的标准木分别取得乔木各部分的干重。采用W=a(D2H)b的幂函数方程,获得每公顷土地上的树干重32.16吨,枝条重9.85吨、叶重1.68吨、根重9.95吨。对灌木和草本植物采用收割法作测定:灌木的地上部分每公顷为1.33吨,地下部分为2.3吨;草本植物的地上部分每公顷为0.15吨,地下部分为0.8吨。所以栓皮栎的地上部分总生物量每公顷为45.17吨,地下部分13.05吨,总计58.22吨。 相似文献
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九种蹄盖蕨科植物配子体的酯酶同工酶分析 总被引:4,自引:1,他引:4
本文培养了蹄盖蕨科9个种即中华蹄盖蕨(Athyriumsinense)带岭蹄盖蕨(A.dalingense)、多齿蹄盖蕨(A.multidentatum)(包括青柄和紫柄2种带岭蹄蕨类型)、东北蛾眉蕨(Lunathyriumpycnosorum)、朝鲜介蕨(Dryoathyriumcoreanum)、山冷蕨(Cystopterissudetica)、假冷蕨(Pseudocystopterisspinulosa)、欧洲羽节蕨(Gymnocarpiumdryopteris)和黑鳞短肠蕨(Alantodiacrenata)的配子体为材料,进行酯酶同工酶的分析,以表明它们的种间差异,其中多齿蹄盖蕨的青柄和紫柄两种类型的酶谱存在明显差异,应考虑紫柄为多齿蹄盖蕨的变型。 相似文献
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Nanomedicine is an emerging field that integrates nanotechnology, biomolecular engineering, life sciences and medicine; it is expected to produce major breakthroughs in medical diagnostics and therapeutics. Due to the size-compatibility of nano-scale structures and devices with proteins and nucleic acids, the design, synthesis and application of nanoprobes, nanocarriers and nanomachines provide unprecedented opportunities for achieving a better control of biological processes, and drastic improvements in disease detection, therapy, and prevention. Recent advances in nanomedicine include the development of functional nanoparticle based molecular imaging probes, nano-structured materials as drug/gene carriers for in vivo delivery, and engineered molecular machines for treating single-gene disorders. This review focuses on the development of molecular imaging probes and engineered nucleases for nanomedicine, including quantum dot bioconjugates, quantum dot-fluorescent protein FRET probes, molecular beacons, magnetic and gold nanoparticle based imaging contrast agents, and the design and validation of zinc finger nucleases (ZFNs) and TAL effector nucleases (TALENs) for gene targeting. The challenges in translating nanomedicine approaches to clinical applications are discussed. 相似文献
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Inhibition of mitochondrial complex I improves glucose metabolism independently of AMPK activation 下载免费PDF全文
Wo‐Lin Hou Jun Yin Miriayi Alimujiang Xue‐Ying Yu Li‐Gen Ai Yu‐qian Bao Fang Liu Wei‐Ping Jia 《Journal of cellular and molecular medicine》2018,22(2):1316-1328
Accumulating evidences showed metformin and berberine, well‐known glucose‐lowering agents, were able to inhibit mitochondrial electron transport chain at complex I. In this study, we aimed to explore the antihyperglycaemic effect of complex I inhibition. Rotenone, amobarbital and gene silence of NDUFA13 were used to inhibit complex I. Intraperitoneal glucose tolerance test and insulin tolerance test were performed in db/db mice. Lactate release and glucose consumption were measured to investigate glucose metabolism in HepG2 hepatocytes and C2C12 myotubes. Glucose output was measured in primary hepatocytes. Compound C and adenoviruses expressing dominant negative AMP‐activated protein kinase (AMPK) α1/2 were exploited to inactivate AMPK pathway. Cellular NAD+/NADH ratio was assayed to evaluate energy transforming and redox state. Rotenone ameliorated hyperglycaemia and insulin resistance in db/db mice. It induced glucose consumption and glycolysis and reduced hepatic glucose output. Rotenone also activated AMPK. Furthermore, it remained effective with AMPK inactivation. The enhanced glycolysis and repressed gluconeogenesis correlated with a reduction in cellular NAD+/NADH ratio, which resulted from complex I suppression. Amobarbital, another representative complex I inhibitor, stimulated glucose consumption and decreased hepatic glucose output in vitro, too. Similar changes were observed while expression of NDUFA13, a subunit of complex I, was knocked down with gene silencing. These findings reveal mitochondrial complex I emerges as a key drug target for diabetes treatment. Inhibition of complex I improves glucose homoeostasis via non‐AMPK pathway, which may relate to the suppression of the cellular NAD+/NADH ratio. 相似文献
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