UPLC-PDA法测定藏药翼首草不同药用部位中齐墩果酸和熊果酸的含量

目的:建立测定藏药翼首草不同药用部位中齐墩果酸和熊果酸含量的方法,并比较其不同部位之间的含量差异。方法:采用超高效液相色谱-光电二极管阵列检测器(UPLC-PDA)测定翼首草不同药用部位(全草、地上部位和地下部位)齐墩果酸和熊果酸含量。色谱柱为Acquity UPLC HSS T3(150 mm×2.1 mm,1.8μm);流动相为甲醇-0.1 mol/L乙酸铵溶液(88∶12,V/V),流速为0.2 m L/min;检测波长为210 nm;柱温为30℃;进样量为5μL。结果:齐墩果酸和熊果酸的检测质量浓度线性范围分别为10.65~1 065μg/m L(r=0.999 6)、18.8~1 880μg/m L(r=0.999 4),平均加样回收率分别为96.95%(RSD=1.24%,n=9)、98.12%(RSD=2.13%,n=9),精密度、稳定性、重复性试验的RSD均小于3%。不同药用部位的齐墩果酸和熊果酸含量的高低整体趋势为地上部位>全草>地下部位;翼首草全草中齐墩果酸和熊果酸平均总量为0.35%,地上部位中为0.56%,地下部位中为0.09%。结论:建立的方法快速、准确可靠、重复性好,适合于藏药翼首草不同药用部位中齐墩果酸和熊果酸含量的测定。翼首草地上部位中齐墩果酸和熊果酸含量较全草、地下部位高,建议使用地上部位入药。     

高效液相色谱法测定石见穿中齐墩果酸及熊果酸的含量

目的建立高效液相色谱法对中药石见穿中的熊果酸及齐墩果酸进行含量测定。方法采用高效液相色谱法,色谱柱Agilent HC18(4.6 mm×250 mm,5μm),流动相A相为0.1%甲酸水溶液,B相为甲醇,A∶B=14∶86,流速为1.0ml/min,柱温20℃,紫外检测波长205 nm,进样量50μl,运行时间为35 min。结果熊果酸和齐墩果酸能够达到基线分离,二者分别在11.55～462.0、5.265～210.6μg/ml,呈良好的线性关系,日内、日间精密度均小于5%(n=3),平均回收率分别为100.47%(RSD=1.95%,n=6)、101.88%(RSD=2.98%,n=6)。结论该法简便、快捷,结果准确、重复性好,可用于石见穿中熊果酸和齐墩果酸的质量控制。     

高效液相色谱法测定胃炎停胶囊中齐墩果酸、熊果酸的含量

目的:建立HPLC法测定胃炎停胶囊中齐墩果酸、熊果酸的含量.方法:以SB-C18柱(4.6 mm×150 mm,5 μm)为分离柱,流动相:甲醇-水(85∶15),检测波长:220 nm.结果:齐墩果酸在0.36～1.80 μg范围内线性关系良好,r=0.9998,样品中齐墩果酸的含量为3.68%(mg/g),其回收率为:97.40%, RSD为2.10%(n=5);熊果酸在0.36～1.44 μg范围内线性关系良好,r=0.9980,样品中熊果酸的含量为6.49%(mg/g), 其回收率为101.21%,RSD为2.40%(n=5).结论:本法简便、准确、可靠.     

基于熵权TOPSIS法综合评价不同产地枇杷叶质量

目的 对不同产地枇杷叶的质量进行综合评价。方法 以不同产地的30份枇杷叶为样品，采用热浸法测定其醇溶性浸出物含量，采用紫外分光光度法分别测定其总黄酮含量和总三萜酸含量，采用高效液相色谱法测定其5个三萜酸类成分（野鸦椿酸、山楂酸、科罗索酸、齐墩果酸及熊果酸）的含量。采用熵权逼近理想排序法（TOPSIS）综合评价不同产地枇杷叶的质量；运用SPSS22.0软件对枇杷叶片重、综合评价值、醇溶性浸出物含量、总黄酮含量、总三萜酸含量及5个三萜酸类成分含量进行双变量相关性分析。结果 30份不同产地枇杷叶中醇溶性浸出物含量为（24.56±0.08）%～(34.85±0.13)%，总黄酮含量为（4.69±0.11）～(14.23±0.27) mg/g，总三萜酸含量为（27.58±0.59）～(63.95±1.27) mg/g，野鸦椿酸、山楂酸、科罗索酸、齐墩果酸、熊果酸的含量分别为（0.728±0.011）～(6.064±0.063)、（0.526±0.013）～(3.245±0.022)、（1.222±0.025）～(8.807±0.094)、（0.856±0.021）～(2.931±0.075)、（...     

HPLC测定不同产地大苞荆芥中的齐墩果酸和熊果酸

目的 采用HPLC法同时测定大苞荆芥中齐墩果酸和熊果酸的含量,并分析不同产地大苞荆芥质量的差别。方法 采用JADE-PAK ODS-AQ色谱柱(250 mm×4.6 mm, 5μm),流动相为甲醇-0.05 mol·L^-1乙酸铵(85:15),检测波长210 nm,柱温30℃。结果 齐墩果酸和熊果酸的线性范围分别为0.108～4.32μg(r²=0.9993,n=6)、0.212～8.48μg(r²=0.9994,n=6),加样回收率与RSD均符合要求。大苞荆芥中齐墩果酸和熊果酸的平均含量分别为0.0686%、0.1186%。结论 所用方法简便、准确、稳定、可靠,可用于大苞荆芥的质量评价。     

高效液相色谱-二极管阵列检测器法测定扛板归不同部位中齐墩果酸和熊果酸的含量

目的:建立测定扛板归不同部位中齐墩果酸和熊果酸含量的高效液相色谱-二极管阵列检测器方法。方法:色谱柱为Kromasil C18柱(4.6 mm×250 mm,5μm),流动相为0.5%磷酸水溶液-甲醇(10∶90),流速0.8 mL.min-1,检测波长210 nm,柱温30℃。结果:齐墩果酸在0.228～2.850μg时,与峰面积呈良好的线性关系(r=0.9998),平均回收率为97.4%,RSD为1.5%(n=6);熊果酸进样量在0.544～6.800μg时,与峰面积呈良好的线性关系(r=0.9998),平均回收率为96.9%,RSD为1.2%(n=6)。结论:方法准确,操作简便,数据可靠,可用于扛板归中齐墩果酸和熊果酸的含量测定。     

HPLC法同时测定毛建草中齐墩果酸和熊果酸的含量

目的建立毛建草中齐墩果酸和熊果酸的高效液相色谱测定方法。方法采用ODS柱,流动相为乙腈-甲醇-水-醋酸铵(70∶14∶16∶0.05),检测波长210nm。结果齐墩果酸在0.196～3.920μg范围内线性关系良好,熊果酸在0.512～12.800μg范围内线性关系良好;该法回收率齐墩果酸为99.5%,熊果酸为100.6%;齐墩果酸RSD为2.0%,熊果酸RSD为2.2%(n=6)。结论为毛建草的含量测定提供了一种快速、准确的方法,为蒙药植物资源的进一步开发提供了依据。     

高效液相色谱-蒸发光散射检测法同时测定木瓜中齐墩果酸和熊果酸含量

目的:建立高效液相色谱-蒸发光散射检测法同时测定中药木瓜中齐墩果酸和熊果酸含量.方法:固定相为YMC C18(4.6 mm×250 mm,5 μm)色谱柱,柱温:35 ℃;流动相:乙腈-水(88∶12),流速:0.8 mL·min-1;蒸发光散射检测器检测,漂移管温度90 ℃,气体(空气)流速2.30 L·min-1.结果:齐墩果酸在0.20～2.01 μg范围内(r=0.999 6)线性关系良好,熊果酸在0.20～2.05 μg范围内(r=0.999 8)线性关系良好.木瓜中齐墩果酸和熊果酸的回收率分别为99.2%和97.8%,RSD分别为2.2%(n=5)和1.4%(n=5).结论:方法简便、准确,重现性好.     

RP-HPLC法同时测定鹿蹄草中齐墩果酸和熊果酸的含量

目的:建立同时测定鹿蹄草中齐墩果酸和熊果酸含量的方法。方法:采用反相高效液相色谱法。色谱柱为Kromasil C18(250 mm×4.6 mm,5μm),流动相为甲醇-水-磷酸(88∶12∶0.15,V/V/V),流速为0.9 ml/min,柱温为30℃,检测波长为210 nm。结果:齐墩果酸进样量在0.462⁴.620μg时,与峰面积积分值呈良好的线性关系(r=0.999 98,n=6),平均加样回收率为98.6%,RSD=2.1%(n=6);熊果酸进样量在1.0644.620μg时,与峰面积积分值呈良好的线性关系(r=0.999 98,n=6),平均加样回收率为98.6%,RSD=2.1%(n=6);熊果酸进样量在1.064¹0.640μg时,与峰面积积分值呈良好线性关系(r=0.999 99,n=6),平均加样回收率为98.5%,RSD=2.2%(n=6)。结论:该方法操作简单、结果准确、重复性好,适用于鹿蹄草中齐墩果酸和熊果酸含量的同时测定。     

反相高效液相色谱法测定药用香薷中齐墩果酸和熊果酸的含量

目的 采用超声辅助提取,建立药用香薷中齐墩果酸和熊果酸的高效液相色谱分析方法.方法 色谱柱为Kromasil C18柱(4.6 mm×250 mm,5μm),流动相为甲醇∶水∶磷酸(90:10:0.1,v/v/v),流速0.8 ml/min,检测波长210 nm,柱温25℃.结果 齐墩果酸在0.228 ～2.850μg时,与峰面积呈良好的线性关系(r =0.9998),平均回收率为97.5％,RSD为1.5％(n=6);熊果酸进样量在0.544～6.800 μg时,与峰面积呈良好的线性关系(r =0.9998),平均回收率为96.9％,RSD为1.2％(n=6).结论 该方法准确,操作简便,数据可靠,可用于香薷中齐墩果酸和熊果酸的含量测定.     

Clevudine University of Georgia/Abbott/Bukwang/Triangle/Yale University

The pyrimidine analog, clevudine (L-FMAU: 2'-fluoro-5-methyl-beta-L-arabinofuranosyluridine) is a potent antihepatitis B virus (HBV) and anti-Epstein-Barr virus (EBV) agent, discovered by researchers at the University of Georgia, in collaboration with Yale University and Bukwang. Bukwang transferred its technology to Triangle Pharmaceuticals in 1998 together with a license to develop clevudine worldwide except Korea [279649], [281942]. In June 1999, Triangle and Abbott Laboratories entered into a strategic alliance to copromote antiviral products including L-FMAU [326798]. In September 2000, Triangle Pharmaceuticals Inc initiated a 30-day phase I/II evaluation of clevudine in HBV-infected patients [381755]. Clevudine is a much less toxic derivative of the toxic agent P-D-FMAU. The mechanism of action of clevudine is not yet clear, but the agent induces a rapid decrease in HBV nucleic acid as doses increase from 0.3 to 10 mg/kg [319145]. It is believed that the target for clevudine lies in the viral replication mechanism. Clevudine is phosphorylated to the triphosphate form intracellularly. This is removed slowly from the cells, thus exerting a sustained inhibitory antiviral activity [178173], [320720], [320721].     

Spotlight from the American Society for Preventive Cardiology on Key Features of the 2018 AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guidelines on the Management of Blood Cholesterol

The 2018 AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Blood Cholesterol retains focus on recommendations for statin treatment in the original four statin-eligible groups [those with atherosclerotic cardiovascular disease (ASCVD), diabetes, low-density lipoprotein cholesterol (LDL-C) ≥ 190 mg/dL, and higher risk primary prevention] without the use of treatment initiation or target LDL-C levels from the earlier 2013 American College of Cardiology/American Heart Association (ACC/AHA) guideline, but has several new features. First, patients with primary prevention are divided into those who are at low (< 5%), borderline (5% to < 7.5%), intermediate (7.5% to < 20%), and high (≥ 20%) risk based on the ASCVD risk estimator. Moreover, the new guideline goes further to consider a wider range of factors [now called “risk enhancers”—premature family history of ASCVD, persistently high LDL-C, chronic kidney disease (CKD), metabolic syndrome, conditions specific to women, inflammatory diseases, and high-risk ethnicities] that can be used to better inform the treatment decision. Moreover, more detailed recommendations on how the results of coronary calcium scanning can be used to inform the treatment decision are provided, including how it may be used to “de-risk” certain patients for delaying or avoiding the use of statin therapy. There are also specific sections for cholesterol management in other patient subgroups including women, children, certain ethnic groups, those with CKD, chronic inflammatory disorders and HIV, as well as discussion on the management of hypertriglyceridemia. Importantly, for persons with known ASCVD, a distinction is made for those who are at “very high risk” based on having had two major ASCVD events or one major event and two or more other high risk conditions, such as diabetes or other major risk factors, or bypass surgery or percutaneous intervention. Finally, the concept of a threshold LDL-C for initiating a non-statin therapy (after considering highest tolerated statin dosage) is provided, with ezetimibe recommended as the key non-statin to be added if the LDL-C still remains ≥ 70 mg/dL for all ASCVD patients, and in those who are at “very high risk”, further consideration for using a proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitor. While the new guideline does have greater detail (and arguably, complexity), the refinements provide a strategy for guiding the clinician to target both statin and non-statin therapy to those most likely to derive benefit.     

Cerebral metabolism of [3H]-p-chloroamphetamine

The time-dependent metabolism of intraventricularly administered $\text{[}{}^3\text{H}\text{]-p-}\text{chloroamphetamine}$ was followed. The parent compound and its metabolites were recovered by high pressure liquid chromatography and characterized by high pressure liquid chromatography, thin-layer chromatography, and gas chromatography-mass spectrometry. By 4 hr after injection, two major toluene-soluble metabolites were present in brain. Their biological half-lives were different from the parent compound. On the basis of their analyses, one of the metabolites is p-chloronorephedrine, the other (P₃) is as yet unidentified. Pretreatment with Lilly 110140 prevented or markedly reduced the synthesis of both p-chloronorephedrine and P₃. Iprindole prevented the synthesis of p-chloronorephedrine. The P₃ appeared first in the brain then in the liver, suggesting that both of these organs can metabolize p-chloroamphetamine to this compound. The metabolites were recovered primarily from the nuclear and microsomal fractions following subcellular fractionation of the brain, with small quantities present in the synaptosomal fraction. The level of metabolites was higher in the brainstem than in the neocortex. Glutathione, administered simultaneously with p-chloroamphetamine either intraventricularly or intraperitoneally failed to alter the toxicity of p-chloroamphetamine.     

Conversion of the N-O-glucuronide and N-O-sulfate conjugates of N-hydroxyphenacetin to reactive intermediates

The N-O-glucuronide of [¹⁴C]acetyl-N-hydroxyphenacetin is sufficiently stable to purify, but slowly breaks down in aqueous solutions to a reactive intermediate that can covalently bind to protein. When the pure compound was incubated in Tris buffer, pH 7.4, at 37°, it decomposed with a half-life of about 8.7 hr to the following compounds: phenacetin, 2-hydroxyphenacetin glucuronide, acetamide and acetaminophen. On addition of glulathione to the systems and allowing the reactions to go to completion, a glutathione-acetaminophen conjugate was formed at the expense of acetamide and acetaminophen: the fraction converted to phenacetin or to the 2-hydroxyphenacetin glucuronide was unchanged. On addition of ascorbic acid to the system and allowing the reactions to go to completion, the fraction converted to acetaminophen was increased at the expense of acetamide: the fractions converted to phenacetin and 2-hydroxyphenacetin glucuronide, however, were again unchanged. When the glucuronide was incubated with bovine serum albumin, covalent binding to the protein occurred at the expense of acetaminophen and acetamide; again, the fraction of the glucuronide converted to phenacetin and 2-hydroxyphenacetin glucuronide was unchanged. Moreover, the covalent binding could be partially prevented by addition of ascorbic acid or glutathione. Since there is formation of covalently bound material, the glutathione conjugate and acetaminophen appear to be interrelated; it seems likely that they are formed from a common intermediate, possibly acetylimidoquinone. However, the data suggest that the formation of phenacetin and 2-hydroxyphenacetin glucuronide occurs by different mechanisms. The N-O-sulfate of [¹⁴C]acetyl-N-hydroxyphenacetin also breaks down to a reactive intermediate that has properties similar to those of the reactive intermediate formed from the N-O-glucuronide and thus may also be N-acetylimidoquinone. By contrast, the relative ability of various nucleophiles to prevent the covalent binding of the reactive intermediate formed from the N-O-sulfate of 2-acetylaminofluorene to protein differs from the relative ability of the nucleophiles to prevent the covalent binding of the reactive intermediate of either the N-O-sulfate or the N-O-glucuronide of phenacetin, suggesting that the relative rates at which these intermediates combine with the different macromolecules may differ markedly.     

甘草配伍大戟的体外肝毒性研究

目的 研究甘草和大戟配伍的体外肝毒性。方法 采用显微观察法和MTT法检测不同浓度的甘草单煎液、大戟单煎液、甘草-大戟合煎液和甘草-大戟单煎混合液对人肝癌细胞HepG2增殖的影响,并比较大戟单煎液、甘草-大戟合煎液和甘草-大戟单煎混合液相当浓度下细胞毒性的大小。结果 大戟单用及大戟与甘草配伍均有细胞毒性,且呈剂量相关性;与大戟单煎液相比,甘草-大戟单煎混合液细胞毒性无明显差异,甘草-大戟合煎液细胞毒性减小。结论 甘草和大戟配伍导致大戟的体外肝毒性减小。     

刺五加的研究进展

刺五加含有苷类、黄酮、多糖等多种活性成分,具有免疫调节、抗肿瘤、抗衰老、抗疲劳等药理作用。对国内外刺五加相关文献进行总结,为刺五加进一步的研究和开发提供参考资料。     

Structure-activity relationships of met5- and leus-enkephalin analogues

1. The effect of various analogues of met5- and leu5-enkephalin were determined on the reduction in twitch height of the electrically-stimulated longitudinal muscle preparation of the guinea-pig ileum and of the isolated mouse vas deferens. 2. In the guinea-pig ileum, D-alanine2-met5-enkephalin was the most potent whereas leu5-enkephalin was the most potent in the mouse vas deferens. 3. The met5-enkephalin analogues were more effective in reducing the twitch height of the ileum than they were in depressing that of the vas deferens preparation. The leu5-enkephalin analogues were more potent in their effects on the mouse vas deferens than they were on the guinea-pig ileum. 4. When a peptide bond is replaced by a glycol bond as in glycol2-3-leu5-enkephalin there is a marked reduction in opiate-like activity. 5. Substitution of a D-alanine residue for the glycine2 residue, as in D-alanine2-met5-enkephalin, increases the duration and potency of opiate-like activity. 6. These results confirm that modification of either met5- or leu5-enkephalin can alter the opiate-like potency of the resulting analogues. It appears that an intact tyrosyl residue of leu5-enkephalin is essential for such activity and that substitution of a D-alanine2 residue for the glycine2 residue confers resistance to enzymatic degradation on the met5-enkephalin peptide. In addition, the glycine2-3 peptide bond is essential for opiate-like activity.     

Quantitative histochemical studies of striatal dopamine depletion following dl-α-methyl-p-tyrosine administration

This study investigated the use of a microfluorimetric histochemical method for the measurement of the depletion of dopamine in the rat caudate nucleus, following α-methyl-p-tyrosine (α-MT) administration. The depletion in three behavioral situations was compared with that of a control group which remained in a cage.The results of the control group indicate that there had been a reduction of approximately 50% in the intensity of the formaldehyde-induced fluorescence derived from dopamine in a region of the neuropil of the caudate nucleus, during the interval (3 hr 40 min) between α-MT, 300 mg/kg i.p., and killing. Disruption of conditioned avoidance response (CAR) performance after α-MT administration was confirmed, but in this study CAR performance in previously trained rats did not have a significant effect on the depletion of formaldehyde-induced fluorescence of the striatal neuropil after α-MT administration. The levels of α-MT-induced depletion of formaldehyde-induced fluorescence in the striatal neuropil following a period of muscular co-ordination/activity and following a period of CAR training were also not significantly different from those shown by a control group.     

Nampt/Visfatin/PBEF研究进展

尼克酰胺磷酸核糖转移酶(nicotinamide phosphoribosyltransferase,Nampt)是生物合成NAD的关键限速酶,又被称为前B细胞克隆增强因子(pre-B cell colony enhancing factor,PBEF)和内脏脂肪素(visfatin).最近研究发现,Nampt/Visfatin/PBEF在NAD生物合成、代谢、炎症反应和细胞增殖、分化、凋亡等诸多领域发挥作用,可能影响2型糖尿病、急性肺损伤、恶性肿瘤等疾病发生、发展和预后.本文主要对Nampt/Visfatin/PBEF的生理功能及临床意义进行综述.