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??OBJECTIVE To clarify the effect of total glucosides from paeony(PTG) on irritable bowel syndrome (IBS), and to explore the molecular mechanism of PTG on alleviating diarrhea symptoms and abdominal pain.METHODS The diarrhea model was conducted by exposing rat to restraint stress stimulation and bellyache model was conducted by subcutaneous injection of neostigmine to mice. Based on these two models, the curative effect of PTG on IBS was investigated. To investigate the regulative effects of PTG on Caco-2 cells, the Caco-2 monolayer cell model with barrier dysfunction was established by trypsin stimulation, and the inflammatory Caco-2 cell model was established by interleukin-1?? (IL-1??) stimulation.RESULTS PTG could significantly reduce the frequency of defecation in diarrhea rat model (P<0.05) and relieve abnormal bowel movements in bellyache mice model (P<0.05). After PTG treatment, the TEER value of Caco-2 monolayer was significantly increased (P<0.01), the transmittance of fluorescence yellow was significantly decreased (P<0.001) and the expression of tight junction (ZO-1)protein was notably up-regulated (P<0.001). In addition, the gene and protein expression of nuclear factor profilin kappa B(I??B??)in inflammatory Caco-2 cell model was significantly improved (P<0.001) after PTG treatment.CONCLUSION PTG significantly ameliorates IBS symptoms by protecting the barrier function of Caco-2 cell monolayer and relieving inflammation of Caco-2 cells.     

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??OBJECTIVE To observe the effect of guhong injection(GHI) on tibial fracture healing in rats and to explore the mechanism of the action of GHI. METHODS One hundred and eighty male SD rats were randomly divided into 6 groups with 30 rats in each group: sham operation group, model group, positive drug group(compound ossotide injection, 5 mL??kg^-1), low, medium and high dose of GHI groups(2.5, 5, 10 mL??kg^-1). In addition to the sham operation group, the other groups established the rat model of tibial fracture. All were given once daily intraperitoneal injections and samples were taken at 1st, 2nd, 4th and 6th week. Blood biochemical analysis and Elisa kit detection were performed on blood samples. X-rays, biomechanical tests, immunohistochemistry and RT-PCR were performed on the tibial samples. RESULTS ??After administration for one, two and four weeks, the levels of serum calcium(Ca) and phosphorus(P) in medium and high dose of GHI groups were higher than those in model group(P<0.05). ??X-ray showed that the outer callus growth and the disappearance of fracture line in all dose groups of GHI were faster than those in model group. ??Compared with model group, the maximum load and rigidity of medium and high dose of GHI groups were increased at each time point(P<0.05), and the trend of stress line graph were improved obviously. ??The content of alkaline phosphatase(ALP) in medium and high dose of GHI groups were higher than that in model group at each time point(P<0.05). Compared with model group, the serum levels of PDGF were increased in all dose groups of GHI(P<0.05 or P<0.01). After administration for one, two and four weeks, the serum BMP-2 in all dose groups of GHI were higher than those in model group(P<0.05 or P<0.01). ??Compared with model group, the expression of Runx2 mRNA were increased in medium and high dose of GHI groups, as well as Smad5 protein expression(P<0.05 or P<0.01). CONCLUSION GHI could significantly improve the biomechanical properties of bone in fracture rats. The promotion of fracture healing might be through the upregulation of PDGF and BMP-2 expression in different stages of bone healing, and the regulation of BMP/Smad5/ Runx2 signaling may be one of the mechanisms of promoting fracture healing.     

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??OBJECTIVE To explore whether QSC can have cardioprotective efficacy after myocardial infarction(MI),we design this experiment in a preclinical model of myocardial infarction in rats. METHODS Four weeks after left anterior descending coronary artery ligation, rats received either intragastric administration of QSC,or the same volume of saline.Male SD rats were given the ligation of anterior descending coronary artery. After 4 weeks,42 male rats were chosen and randomly divided into 3 groups. The model group(normal saline solution for 4w, n=14), low-dose control group(5??10⁴ mg??kg^-1??d^-1 of drug QSC, for 4w, n=14), and QSC moderate dose group(10??10⁴ mg??kg^-1??d^-1 of QSC for 4w,n=14). The sham-operation group(n=16) was only given treatment of chest-open without ligation of anterior descending coronary artery,divided into 2 groups,the Sham-group(normal saline solution for 4w,n=8)and Sham+QSC group(5??10⁴ mg??kg^-1??d^-1 of drug QSC,for 4w,n=8).Cardiac function was assessed echo cardio-graphically.Angiogenesis and apoptosis were detected using histology and Western blot methods four weeks after QSC therapy. RESULTS Reductions in infarction area and scar collagen content in MI+QSC group were observed in the infarct region compared with the saline control and MI+QSCL group. QSC also improved cardiac function after treatment. QSC significantly decreased apoptosis relative to control group, evidenced by influencing the expression of Bcl-2, Bax, cytochrom C and caspase-3 in the myocardial infarction. Meanwhile, angiogenesis in the infarctive regions were significantly enhanced relative to control group, evidenced by increased density of a-smooth muscle actin and CD31 positive vessels respectively. Similarly, the mRNA expressions of VEGF and HIF-1?? were up-regulated.Additionally. OSC involvement also increased the phosphorylation of AKT and down-regulated the phosphorylation of MEK/ERK. CONCLUSION There is no significant difference between QSC low-dose group and the model group, but QSC moderate dose group can improve cardiac function in rats after MI, the underlying mechanism of which can be explained by increasing angiogenesis,reducing apoptosis partially via the activation of AKT signaling pathway and inhibition of phosphorylation of MEK/ERK.     

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??OBJECTIVE To investgate the protective effects and mechanisms of Polygonatum kingianum on nonalcoholic fatty liver induced by high-fat diet in rats. METHODS A total of 42 rats were randomly divided into normal control group (normal saline), model group (normal saline), resveratrol group (positive control, 40 mg??kg^-1) and low-, middle-and high-dose P. kingianum group (1, 4, 8 g??kg^-1). They were intragastrically given corresponding compounds (or normal saline) once a day, lasting for 14 weeks. Nonalcoholic fatty liver was induced by feed with high-fat diet for 14 weeks in those groups except for normal control group. Blood was taken from the corneas at 0, 6, 12 and 14 week, and then the levels of triglyceride (TG) and total cholesterol (TC) in serum were determined. Afterword, the rats were sacrificed at 14 week followed by the measurement of organs indices of liver??spleen and kidney, as well as the detection of levels of TC, TG, high density lipoprotein cholesterol (HDL-C) and low density lipoprotein cholesterol (LDL-C) in liver tissues. Furthermore, the levels of malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GSH-PX), ATP synthase and respiratory chain complex ?? and ?? in hepatic mitochondria were determined. RESULTS Nonalcoholic fatty liver was successfully induced by high-fat diet in rats. The different doses of water extract of P. kingianum could significantly inhibit the increasing of liver index and serum TC in high-fat diet-induced rats, alleviate swelling, degeneration, necrosis and inflammatory injury of hepatic cells, inhibit the increasing of TC, TG and LDL-C and decrease of HDL-C in liver tissues, as well as inhibit the exaltation of MDA level and reduction of SOD, GSH-PX, ATP synthase and respiratory chain complex ?? and ?? activity in hepatic mitochondria. CONCLUSION P. kingianum shows protective effects on high-fat diet-induced nonalcoholic fatty liver in rats. The action mechanism may be related to the elimination of oxidative stress product (MDA) and improvement of antioxidant enzyme activity (SOD and GSH-PX) in hepatic mitochondria, as well as the improvement of energy metabolism obstacle.     

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??OBJECTIVE To investigate the influence and mechanism of different doses of Yangxinshi on infarction region angiogenesis of Wistar rats after acute myocardial infarction. METHODS Sixty healthy male Wistar rats were randomly divided into five groups, named as follow:group A: rosuvastatin group (0.75 mg??kg^-1??d^-1), group B: high-dose Yangxinshi(0.27 g??kg^-1??d^-1),group C:mid-dose Yangxinshi group (0.18 g??kg^-1??d^-1),group D: Low-dose Yangxinshi group (0.09 g??kg^-1??d^-1),group E:saline control group. A, B, C, D group was respectively given the drug by gavage, group E received normal saline by gavage. The models of acute myocardial infarction can be established in the forth week . After continued drugs for 4 weeks, rats were killed before detected blood biochemicalindexes such as blood lipids, liver and kidney function. Myocardial tissue was sliced and stained infarcted myocardium by HE to observe the pathological changes, also extract ischemic and infarct myocardium tissue protein and test VEGF protein expression with immunohistochemistry. RESULTS Myocardial tissue HE staining were observed a lot of survival island cardiomyocytes and neonatal thin-walled capillaries in four treatment groups , however,control group exist less normal cardiomyocytes and capillaries mainly disappear. Immunohistochemistry RESULTS showed high-doses of Yangxinshi group express higher VEGF protein compared with mid-dose group, low-dose group and control group, the difference was statistically significant (P<0.05), VEGF protein expression was significantly increased the in mid-dose and high-dose Yangxinshi groups than rosuvastatin group, the difference was statistically significant (P<0.05). CONCLUSION Yangxinshi promote production of VEGF protein and angiogenesis of ischemic myocardium ,in addition its role and its dose is positive correlated. VEGF protein expression was significantly increased the in mid-dose and high-dose Yangxinshi groups than rosuvastatin group, the difference is statistically significant (P<0.05).     

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??OBJECTIVE To abserve the antidepressant effect and mechanism of honokiol on acute and chronic stress mouse. METHODS Forced swimming model of acute stress (FST) and chronic stress mice model were used. The acute stress mouse were randomized into a control group, a fluoxetine group (3.3 mg??kg^-1), honokiol groups (2.5,5,10 mg??kg^-1). The chronic stress mouse were randomized into a blank group, a model group, a fluoxetine group(3.3 mg??kg^-1), honokiol groups (2.5,5,10 mg??kg^-1). Then, the immobility time of forced swimming, 5-hydroxytryptamine (5-HT) and 2,3- indole dioxygenase (IDO) contents in mouse brain tissue by Elisa Kit, and the expression of IDO mRNA in brain tissue used by quantitative real-time PCR were studied. RESULTS ??After acute stress, the immobility time of forced swimming in each treatment group was significantly shorter than that in the model group (P<0.05). The 5-HT content of fluoxetine and honokiol medium and high dose group was significantly higher than that of model group (P<0.05, P<0.01). The IDO content of honokiol high dose group was significantly higher than that of model group (P<0.05). ??After chronic stress, the immobility time of the model group were significantly higher than the blank group (P<0.01). The 5-HT content in brain tissue of the model group was significantly lower than that of the blank group (P<0.01), the IDO content in brain tissue and its expression level of mRNA increased comparing with the normal group (P<0.01). For each treatment group, the immobility time of forced swimming, IDO content and the expression level of IDO mRNA was significantly decreased, and the 5-HT content was significantly increased, comparing with the model group with significant difference (P<0.05). CONCLUSION Honokiol can relieve the depression behavior of mouse and have certain antidepressant effect. The main mechanism may be associated with the increase of 5-HT, reduction of the tryptophan pathway enzyme IDO content and its gene expression level.     

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??OBJECTIVE To evaluate the inhibitory effects and mechanism of Hydrochloric acid chlorobenzene sulperzon (HACS) on neuronal inflammation were studied in order to evaluate possible application of it in AD therapy. METHODS The release of NO (nitric oxide) by astrocyte was detected by Griess methods and the chemotaxis of mouse macrophage was detected by Boyden chemotaxis chamber. The cell viability was detected by MTT assay. The content of IL-6 and RANTES (T cell expressed and presumably secreted)was determined by ELISA. The expression of mRNA of IL6 and RANTES was detected by RT-PCR. The intracelluar Ca²⁺ was detected by confocal microscope. RESULTS HACS efficiently decreased the release of NO from astrocyte stimulated by LPS (1 ??g??mL^-1), chemotaxis of mouse macrophage stimulated by PAF (5??10^-8 mol??L^-1), expression of IL-6 and regulated upon activation of RANTES in U251 cells induced by IL-1?? (50 ng??mL^-1). In addition, HACS significantly inhibited the increase of intracellular Ca²⁺ in U251 cells induced by A??1-42(50 ??g??mL^-1)/ sodium glutamate(100 ??mol??L^-1)or IL-1??(50 ng??mL^-1). CONCLUSION HACS efficiently inhibites the activation of astrocyte by regulation of intracelluar Ca²⁺inhibition of chemotaxis and decrease of inflammatory cytokines. Especially, the inhibition of RANTES and intracelluar Ca²⁺ induced by inflammatory mediators by HACS is firstly reported in this study.     

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??OBJECTIVE To explore the antibacterial activity and mechanism of fusidic acid combined with aztreonam on 12 clinical isolates of carbapenem-resistant Pseudomonas aeruginosa (CRPA). METHODS Broth dilution method was used to determine the minimum inhibitory concentration(MIC) of the fusidic acid and aztreonam combination.The MIC of two drugs combination were measured by the checkerboard method and partial inhibitory concentration index (FIC) was calculated to determine the combined effect.The synergistic effect of two drugs was assessed by the disk diffusion susceptibility test and the time-killing curves.Extracellular enzyme activity assay was used to detect the strains extracellular enzyme activity changes of fusidic acid alone and combined with aztreonam. The probable mechanism of the combined use of two drugs was discussed. RESULTS Fusidic acid and aztreonam combination displayed synergistic and additive activity on 61.54% and 38.46% isolates, no antagonism activity was observed.The bacteriostasis circle was obviously increased in two drugs combination, of which 41.67% of the strains were changed from drug resistance to sensitive. The time-killing curves showed that the combined of two drugs had bactericidal effect on the isolate PA 320.Extracellular aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH) activity were all increased in a significant difference with the combination of two drugs. CONCLUSION Fusidic acid combined with aztreonam on CRPA is showed synergistic and additive activity in vitro. The mechanism of two drugs in combination may concern with aztreonam help the fusidic acid to overcome the natural hydrophobic antibiotic permeability barriers of gram-negative bacteria.     

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??OBJECTIVE To investigate vasodilation effect and mechanism of OW1 was investigated on rat aorta, renal artery, cerebral middle artery, coronary artery, pulmonary artery and mesenteric artery. METHODS Isometric tension was measured in a 610 M-DMT Wire Myograph System. 60 mmol??L^-1 KCl was added to the baths to induce pre-contraction of the 6 arteries. The concentration-response curves of OW1 were constructed on endothelium-denuded aorta rings or blocking endothelial, beta adrenergic receptor, three potassium channels and changing the concentration of intracellular or external calcium respectively. RESULTS OW1 could relax the 6 arteries completely, and E_max were all above 95%. pEC₅₀ were (6.11??0.09), (5.76??0.01), (6.22??0.08), (5.78??0.05), (5.65??0.01), and (6.59??0.07) respectively. ??-Adrenoceptor, ATP sensitive potassium channel and inwardly rectifying potassium channel were not involved in the vasodilatation, whereas blockage of calcium-activated potassium channel with tetraethylammonium had effect. OW1 could inhibit the influx of extracellular calcium and the release of intracellular calcium, thereby inhibiting vasoconstriction. CONCLUSION OW1 could relax the six arteries. The possible mechanisms of the vasodilatation are mainly involved with inhibiting voltage dependent calcium channel and receptor-mediated Ca²⁺ influx and release, and might be partly due to opening calcium-activated potassium channel.     

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??OBJECTIVE To study the anti-leukemia activities and mechanisms of bergenin derivative D-23. METHODS CCK-8 method was applied to investigate anti-tumor activities of D-23. Flow cytometry and immunofluorescence assay were used to observe the effects of D-23 on the apoptosis and autophagy in K562 and Jurkat human leukemia cell lines. Western blot analysis was used to investigate the mechanisms that compound D-23 induced tumor cell apoptosis and autophagy. RESULTS Bergenin derivative D-23 could significantly inhibit the proliferation of K562 and Jurkat cells by inducing cell apoptosis and autophagy. The mitochondrial membrane potential was decreased,protein kinase B(Akt)and heat shock protein 70 (Hsp70) were inhibited,and the expressions of apoptotic related proteins caspase 3 and caspase 9 were activated. In addition, mammalian target of rapamycin (P-mTOR)(Ser 2448 and Ser 2481)protein was inhibited. CONCLUSION Bergenin derivative D-23 shows obvious anti-leukemia activities by inducing cell apoptosis and autophagy. The apoptosis may be associated with the reduction of mitochondrial membrane potential and activation of caspase pathway. The autophagy may be related to the inhibition of Akt/mTOR signaling pathway.     

藓生马先蒿化学成分研究(Ⅱ)

从藓生马先蒿全草分得4个糖甙化合物,根据理化常数及光谱分析鉴定为1个木脂素甙和3个单萜环烯醚甙:丁香醇-4″-O-β-D-吡喃葡萄糖甙、胡麻甙、糙苏甙Ⅱ和山栀子甙。     

藓生马先蒿的化学成分研究

从四川省马边彝族自治县治疗蛇伤有效秘方主要组分之一的藓生马先蒿全草中分离得到4个成分。经理化常数和光谱分析鉴定为马先蒿甙、D-甘露醇、花生酸和三十一碳烷。     

管花肉苁蓉的苯乙醇苷类成分

采用各种色谱技术主要为ＨＰＬＣ从国产管花肉苁蓉Ｃｉｓｔａｎｃｈｅ ｔｕｂｕｌｏｓａ （Ｓｃｈｅｎｋ）Ｗｉｇｈｔ中分离得到７个苯乙醇苷类化合物,根据理化性质和波谱 数据鉴定它们的结构为２′－乙酰基类叶升麻苷（Ⅰ）、类叶升麻苷（Ⅱ）、ｃｒｅ－ｎａｔｏｓｉｄｅ（Ⅲ）、丁香苷Ａ３／′－α－Ｌ－吡喃鼠李糖苷（Ⅳ）、异类叶升麻苷（Ⅴ）、去咖啡酰基类叶升麻苷（Ⅵ）和红景天苷（Ⅶ）。化合物Ⅲ为首次从本属植物中分离得到,其它化合物为首次从本植物中分离得到。     

肉苁蓉苯乙醇总苷对高原脑水肿大鼠水通道蛋白4的影响

目的:观察肉苁蓉苯乙醇总苷预防给药对高原脑水肿模型大鼠的作用。方法:大鼠随机分为正常对照组、模型组、大花红景天口服液组(1.78 m L·kg-1·d-1),肉苁蓉苯乙醇总苷低、中、高剂量组(75、150、300 mg·kg-1·d-1),每组12只,灌胃预防给药10 d,第8天起除正常对照组外其余各组置于模拟海拔5000 m高原环境72 h建立高原脑水肿模型,观察各组大鼠脑组织病理改变,检测脑组织干湿比、脑组织水通道蛋白4(aquaporin-4,AQP4)的表达变化。结果:与正常对照组(脑组织干湿比为:4.65±0.10)相比,模型组大鼠脑组织干湿比(5.14±0.16)显著升高,脑组织AQP4表达增加(模型组表达为正常组的2.21±0.46倍)。肉苁蓉苯乙醇苷能够降低脑组织含水量(低中高剂量组依次为:4.68±0.08,4.66±0.10,4.66±0.18),且能降低高原脑水肿大鼠脑组织水通道4mRNA(低中高剂量组依次为正常组的:1.20±0.30,1.03±0.17,1.12±0.33倍)和蛋白的表达,改善高原脑水肿大鼠脑水肿病理改变。结论:肉苁蓉苯乙醇苷能够预防高原脑水肿的发生,可能与其抑制水通道4的表达有关。     

肉苁蓉苯乙醇苷对大鼠高原肺水肿的防治作用

目的：探讨健脾益肠散对溃疡性结肠炎（UC）大鼠髓样分化因子88（MyD88）的影响。方法：将60只大鼠随机分为正常组、模型组、柳氮磺吡啶组（0.3 g·kg^-1）及健脾益肠散高（204 g·kg^-1）、中（136 g·kg^-1）、低剂量（68 g·kg^-1）组,每组10只;除正常组外,其余均采用2,4,6-三硝基苯磺酸（TNBS）/乙醇法复制UC大鼠模型;灌胃给药21 d后,用ELISA、免疫组化、Western blot及RT-PCR法检测各组大鼠血清MyD88含量和结肠组织MyD88的表达。结果：模型组大鼠血清MyD88水平及结肠组织MyD88蛋白和mRNA表达均明显高于正常组（P<0.01）;健脾益肠散高、中剂量组血清MyD88含量和结肠MyD88蛋白及mRNA表达均较模型组降低,差异有统计学意义（P<0.05或P<0.01）;健脾益肠散低剂量组MyD88蛋白表达亦低于模型组（P<0.05）;健脾益肠散高剂量组对MyD88的影响与柳氮磺吡啶组比较差异不显著,但明显优于低剂量组（P<0.05）。结论：健脾益肠散对UC肠黏膜免疫的保护作用可能与降低外周血MyD88水平及结肠组织MyD88的蛋白和基因表达有关。     

盔状黄芩中的苯乙醇苷及黄酮苷类化合物分析

目的:研究盔状黄芩全草的化学成分。方法:取干燥的盔状黄芩全草,粉碎后用95%乙醇回流提取,减压浓缩得总浸膏。将浸膏悬浮于水中,依次用石油醚、三氯甲烷、乙酸乙酯、正丁醇进行萃取,得石油醚、三氯甲烷、乙酸乙酯和正丁醇部位,取乙酸乙酯部位分别用硅胶柱色谱,Sephadex LH-20柱色谱及高效制备薄层等方法对盔状黄芩中的苷类化合物进行分离纯化,并根据理化性质和波谱数据对其化学结构进行阐明。结果:从乙酸乙酯部位共发现11个化合物,包括9个苯乙醇苷和2个黄酮苷,分别为isocrenatoside(1),osmanthuside B6(2),eutigoide A(3),plantainoside C(4),calceorioside B(5),isomartynoside(6),verbascoside(7),acteoside(8),desrhamnosyl acteoside(9),5,7-二羟基-8,2'-二甲氧基-7-O-β-D-葡萄糖苷(10),洋芹素-7-O-鼠李糖苷(11)。结论:化合物1~4,7~11为首次从该植物中发现;同时,文献调研发现,分离得到的plantainoside C,洋芹素-7-O-鼠李糖苷等化合物具有一定的抗炎、抗氧化活性,为进一步开展盔状黄芩的药效物质基础研究及该药材的开发利用提供了很好的参考依据。     

苁蓉总苷对小鼠学习记忆障碍的影响

目的观察苁蓉总苷对东莨菪碱所致的小鼠学习记忆获得障碍及亚硝酸钠所致小鼠学习记忆巩固障碍的影响.方法使用跳台法观察小鼠的学习记忆功能.连续灌胃给予苁蓉总苷30d,于实验的第29天训练,第30天测试,记录各动物的首次跳台潜伏期及5 min内的错误次数.东莨菪碱模型于训练前15 min腹腔注射东莨菪碱,而亚硝酸钠模型于训练后立即皮下注射亚硝酸钠.结果与东莨菪碱模型组比较,苁蓉总苷400、200 mg/kg组及脑复康组潜伏期均明显延长,错误次数明显减少;苁蓉总苷100 mg/kg组潜伏期亦明显延长,但错误次数只有一定程度的减少.与亚硝酸钠模型组比较,苁蓉总苷400、200 mg/kg组潜伏期均明显延长,错误次数有一定程度的减少,但无统计学意义;苁蓉总苷 100 mg/kg组潜伏期及错误次数只有一定程度的改善;脑复康组潜伏期明显延长,错误次数显著减少.结论苁蓉总苷对东莨菪碱所致的小鼠学习记忆获得障碍及亚硝酸钠所致小鼠学习记忆巩固障碍均有明显的改善作用.     

羊肚参的化学成分研究

目的 研究羊肚参(亨氏马先蒿Pedicularis henryi)的化学成分。方法 采用Sephadex LH-20、RP18、MCI-gel CHP-20P、半制备型HPLC色谱等方法进行分离纯化,根据理化性质及波谱数据鉴定化合物的结构。结果 从羊肚参根95%乙醇提取物中分离得到了9个化合物,分别鉴定为syringaresinol mono-β-D-glucoside(1)、车前醚苷(2)、苯乙酸(3)、2″,3″-乙酰马蒂罗苷(4)、cis-2″,3″-O-acetylmartynoside(5)、地黄苷(6)、cis-martynoside(7)、leucoseceptoside A(8)、焦地黄苯乙醇苷D(9)。结论 化合物1~9均为首次从该植物中分离得到。     

甘肃马先蒿毛蕊花糖苷和异毛蕊花糖苷制备工艺研究

目的建立制备甘肃马先蒿中毛蕊花糖苷和异毛蕊花糖苷单体的方法。方法以毛蕊花糖苷和异毛蕊花糖苷质量分数为考察指标,通过静态吸附和动态解吸附实验,从01A1、D101、HPD100、AB-8、XAD-6、DM130、DM-301、DM-201、YWD06B及YWD06C中筛选出最佳树脂,确定制备甘肃马先蒿总苯乙醇苷的最佳纯化工艺。并以中压柱色谱技术分离制备毛蕊花糖苷和异毛蕊花糖苷单体,根据波谱数据鉴定结构。结果最佳纯化工艺为上样溶液含生药20 mg/m L,上样体积流量为3 BV/h,先用3 BV的水除杂,再用5 BV 50%乙醇以2 BV/h的体积流量洗脱,洗脱液减压浓缩,冷冻干燥,得甘肃马先蒿总苯乙醇苷纯化物,该纯化物中毛蕊花糖苷和异毛蕊花糖苷的质量分数为42.29%和28.51%。经中压柱色谱精制后分离制备的毛蕊花糖苷和异毛蕊花糖苷单体质量分数分别为98.33%和99.24%。结论该方法高效快速、经济简单、易于实现,可用于毛蕊花糖苷和异毛蕊花糖苷单体的制备。     

车前草中总苯乙醇苷提取工艺研究

目的:筛选车前草中总苯乙醇苷提取的最佳工艺。方法:以总苯乙醇苷的量为指标,采用单因素试验和正交试验优化车前草中总苯乙醇苷最佳提取工艺。结果:车前草中总苯乙醇苷的最佳提取工艺为:车前草粉末(过2号筛)加入25倍量、50%的乙醇并调节p H值为5,于95℃加热回流提取两次,每次120 min。结论:研究结果表明,该提取工艺简单、可靠、重复性好,为车前草的进一步深度开发奠定基础。