高效液相色谱法测定力补金秋胶囊中人参皂苷Rgl和人参皂苷Re含旦里

目的：建立力补金秋胶囊中人参含量测定方法。方法：采用HPLC法测定人参中的人参皂苷Rgl和人参皂苷Re的含量。用Hypersil—C18柱．流动相为乙腈-0．1％磷酸溶液（19．6：80．4）．检测波长为203nm。结果：该方法的线性范围为：人参皂苷Rgl：0.495～3．7125μg．r=0．9998．人参皂苷Re：0．450～3．375μg．r=0．9999。平均回收率分别为：98．28%，97．55％。结论：本方法简便可行．重现性好，可用于该制剂的质量控制。     

同时测定参附注射液二组份含量方法学研究

目的:建立同时测定参附注射液中人参皂苷Rg1和人参皂苷Re的含量方法.方法:高效液相色谱法,Nova Pak C18柱,流动相:乙腈:水(70:30),检测波长:203nm.结果:人参皂苷Rg1和人参皂苷Re分别在0.7208μg～7.208μg(r=0.9997,n=6)和0.6032μg～6.032μg(r=0.9997,n=6)范围内具有良好的线性关系.加样回收率分别为99.6%(RSD=1.2%)和99.8%(RSD=1.3%).结论:该方法准确,灵敏,便捷,可同时控制参附注射液中人参皂苷Rg1和人参皂苷Re的含量.     

超高效液相色谱法测定祛瘀生新胶囊胶囊中人参皂苷Rg1、Rb1及Re

目的：探讨超高效液相色谱法测定祛瘀生新胶囊中人参皂苷Rg1、Rb1及Re。方法：选用LC-20A型超高效液相色谱仪、流动相A:0.1%甲酸水溶液,流动相B:甲醇,梯度洗脱,进样量5μL,流速0.25mL/min,柱温30℃,检验波长203nm,检测祛瘀生新胶囊胶囊中人参皂苷Rg1、Rb1及Re含量。结果：人参皂苷Rg1、Rb1、Re质量浓度分别在19.85～186.73μg/mL、25.39～261.40μg/mL、16.02～142.48μg/mL范围内与峰面积有良好的线性关系。人参皂苷Rg1、Rb1、Re精密度在0.8%～1.3%,仪器精密度良好,稳定性为1.2%～1.6%,供试品溶液室温条件下稳定性良好,重复性为1.8%～2.1%,该方法重复性良好,三种成分回收率为96.10%～99.45%,符合要求,3种成分中人参皂苷Rb1含量最少,为0.17mg/g,人参皂苷Re含量最多,为0.31mg/g。结论：高效液相色谱法测定祛瘀生新胶囊胶囊中人参皂苷Rg1、Rb1及Re含量简便可靠,重复性、稳定性好,精密度高,可作为该制剂中人参皂苷检测方法。     

HPLC法测定通心络颗粒剂中人参皂苷Rg1、人参皂苷Re和人参皂苷Rb1的含量

目的 建立通心络颗粒剂中人参皂苷Rg1、人参皂苷Re和人参皂苷Rb1的含量测定方法.方法 采用C18柱,以乙腈-水为流动相进行梯度洗脱,对制剂中人参皂苷Rg1、Re和Rb1进行定量测定,检测波长203nm,流速为1.2mL·min-1,柱温为30℃.结果 人参皂苷Rg1在1.835～18.350μg范围内与色谱峰面积呈线性关系;平均加样回收率98.3%;RSD为1.55%.人参皂苷Re在1.577～15.770μg范围内与色谱峰面积呈线性关系;平均加样回收率98.8%;RSD为1.71%.人参皂苷Rb1在2.334～23.336μg范围内与色谱峰面积呈线性关系;平均加样回收率101.8%;RSD为1.86%.结论 该方法准确度高,重现性好,应用性强,可作为该产品的质量控制方法.     

HPLC法同时测定人参北芪片中人参皂苷Rg1和人参皂苷Re的含量

目的 建立测定人参北芪片中人参的有效成分人参皂苷Rg1和人参皂苷Re的高效液相色谱(HPLC)测定方法.方法 采用ODS-2HYPERSIL柱(250mm×4.6mm 5μm);乙腈-0.1%磷酸溶液(20: 80)为流动相;检测波长为203nm;流速1.0ml/min;柱温35℃.结果 人参皂苷Rg1在0.2024～5.0600μg具有良好的线性关系( r=0.9995),平均回收率为99.0%,RSD为1.04%(n=9);人参皂苷 Re在0.2152～5.3800μg的范围具有良好的线性关系 (r=0.9998),平均回收率为98.2%,RSD为0.70%(n=9).结论 本法快速、准确,可同时测定人参北芪片中人参皂苷Rg1、人参皂苷Re的含量.     

HPLC-ELSD法测定参银颗粒中人参皂苷Rg1及Re的含量

目的：用HPLC～ELSD法测定参银颗粒中人参皂苷Rgl及Re的含量。方法：色谱柱填料为十八烷基键合硅胶,流动相为乙腈-水;温度40℃,气体压力3．5bar。结果：人参皂苷Rgl及Re分别在0．9012～9．012,1．219—12．19μg之间呈良好的线性关系;参银颗粒中2种成分的平均回收率分别为98．2％（RSD1．3％）,97．8％（RSD1．5％）;结论：该方法简便、准确、分离效果好,无干扰,可用于参银颗粒的质量评价。     

HPLC法测定三七水煎液中三七皂苷R_1、人参皂苷Rg_1和Re的含量

目的建立三七水煎液中三七皂苷类成分的含量测定方法。方法采用高效液相色谱法,以乙腈-水(20∶80)为流动相,于203nm检测三七皂苷R1、人参皂苷Rg1和人参皂苷Re的含量。结果三七皂苷R1在0.144～2.64μg(r=0.9995),人参皂苷Rg1在0.10～12μg(r=0.9997),人参皂苷Re在0.15～1.4μg(r=0.9998)范围内,线性关系良好。平均回收率在97%～100%。结论方法简便,快速,重现性好,可作为三七水煎液的质量控制标准。     

HPLC法同时测定人参固本丸中人参皂苷Rg1和人参皂苷Re的含量

目的 建立了测定人参固本丸中的有效成分人参皂苷Rg1和人参皂苷Re的高效液相色谱测定方法.方法 采用UltimateTM XB-C18柱(250mm×4.6mm 5μm);乙腈-0.1%磷酸溶液(20∶80)为流动相;检测波长为203nm;流速1.0mL·min-1;柱温35℃.结果 人参皂苷Rg1在0.0752μg~1.8800μg具有良好的线性关系(r=0.9996),平均回收率为97.8%,RSD为0.011%(n=9);人参皂苷Re在0.1887μg~4.7175μg的范围具有良好的线性关系(r=0.9992),平均回收率为98.2%,RSD为0.015%(n=9).结论 本法快速、准确,可同时测定人参固本丸中人参皂苷Rg1、人参皂苷Re的含量.     

HPLC法同时测定人参北芪片中人参皂苷Rg1和人参皂苷Re的含量

目的建立测定人参北芪片中人参的有效成分人参皂苷Rg1和人参皂苷Re的高效液相色谱（HPLC）测定方法。方法采用ODS-2HYPERSIL柱（250mm×4.6mm5μm）;乙腈-0.1%磷酸溶液（20∶80）为流动相;检测波长为203nm;流速1.0ml/min;柱温35℃。结果人参皂苷Rg1在0.2024～5.0600μg具有良好的线性关系（r=0.9995）,平均回收率为99.0%,RSD为1.04%（n=9）;人参皂苷Re在0.2152～5.3800μg的范围具有良好的线性关系（r=0.9998）,平均回收率为98.2%,RSD为0.70%（n=9）。结论本法快速、准确,可同时测定人参北芪片中人参皂苷Rg1、人参皂苷Re的含量。     

益气降糖胶囊的质量标准研究

目的建立益气降糖胶囊的质量标准。方法采用TLC法对处方中的黄芪、人参、黄连进行定性鉴别;采用HPLC法测定制剂中人参皂苷Rgl和Re的含量。结果TLC法可检出黄芪、人参、黄连的特征斑点;人参皂苷Rgl的线性范围为0．4020-4．0200μg（r=0.9999）,平均回收率为99．5l％（R．妨=1．21％,n=6）;人参皂苷Re的线性范围为0．2040-2．0400μg（r=0．9999）,平均回收率为99．26％（RSD=1．33％,n=6）。结论本质量标准可有效地控制益气降糖胶囊的质量。     

Vascular sphingosine-1-phosphate S1P1 and S1P3 receptors

The sphingolipid sphingosine-1-phosphate (S1P) acts on five subtypes of G-protein- coupled receptors, termed S1P(1) (formerly endothelial differentiation gene-1 [Edg-1]), S1P(2) (Edg-5), S1P(3) (Edg-3), S1P(4) (Edg-6) and S1P(5) (Edg-8), and possibly several other "orphan" receptors, such as GPR3, GPR6 and GPR12. These receptors are coupled to different intracellular second messenger systems, including adenylate cyclase, phospholipase C, phosphatidylinositol 3-kinase/protein kinase Akt, mitogen-activated protein kinases, as well as Rho- and Ras-dependent pathways. Consistently with this receptor multiplicity and pleiotropic signaling mechanisms, S1P influences numerous cell functions. S1P(1)1, S1P(2) and S1P(3) receptors are the major S1P receptor subtypes in the cardiovascular system, where they mediate the effects of S1P released from platelets, and possibly other tissues (such as brain). Thus S1P(1) and S1P(3) receptors enhance endothelial and vascular smooth muscle cell proliferation and migration, playing a key role in developmental and pathological angiogenesis. In contrast, S1P(2) receptors inhibit migration of these cell types, probably because of their unique stimulatory effect on a GTPase-activating protein inhibiting the activity of Rac. S1P receptors can also cause relaxation and constriction of blood vessels. The former effect is mediated by pertussis toxin-sensitive receptors (possibly S1P(1)) located on the endothelium and stimulating phosphatidylinositol 3-kinase/Akt/endothelial nitric oxide synthase (eNOS). The vasoconstricting effect of S1P is likely to be mediated by S1P(2) and/or S1P(3) receptors, via Rho-Rho-kinase, and is more potent in coronary and cerebral blood vessels. Finally, S1P also protects endothelial cells from apoptosis through activation of phosphatidylinositol 3-kinase/Akt/eNOS via S1P(1) and S1P(3) receptors. The variety of these effects, taken together with the existence of multiple receptor subtypes, provides an abundance of therapeutic targets that currently still await the development of selective agents.     

Antimykobakterielle 1-Phenyl-1-alkylaminoalkane

Antimycobacterial 1-Phenyl-1-alkylaminoalkanes Synthesis and testing for antimycobacterial properties (M. tuberculosis H 37 Ra, Middlebrook-7H9-broth) of 1-phenyl-1-alkylaminoalkanes, which differ from antimycobacterial N-alkylbenzylamines by an additional alkyl chain in α-position, is described. By variation of both alkyl chains and introduction of one or two Cl-substituents in the aromatic ring the activity increases up to an optimum within the homologous series. Overstepping optimal lipophilicity or ramification of the alkyl chains decrease activity. Compounds 19, 20, 33-35, 51-53, 61-63, 65-67, 70-73, 96 and 102 - 104 inhibit the growth of M. tuberculosis in concentrations of 2 to 4 μg/ml.     

Sulfation of iodothyronines by human sulfotransferase 1C1 (SULT1C1)*

Sulfation is an important component of human thyroid hormone metabolism. The role of the human sulfotransferase 1C1 (SULT1C1) is not known. Because SULT1C1 is present in the adult thyroid, intra-thyroidal sulfation of thyroid hormones and their metabolites might occur. We tested this hypothesis by determining the ability of recombinant human SULT1C1 to catalyze iodothyronine sulfation. Apparent K(m) values for 3,3',5-triiodothyronine (T(3)), 3, 3'-diiodothyronine (3,3'-T(2)), 3',5',3-triiodothyronine (rT(3)), and 3,3',5,5'-tetraiodothyronine (T(4)) with SULT1C1 were 28.7, 10.3, 10.2, and 59.3 microM, respectively. Thermal stability and responses to inhibitors also were tested with T(3) as the substrate. Enzyme aliquots were measured simultaneously to determine SULT1C1 substrate preferences at optimal iodothyronine concentrations. SULT1C1 activity obtained with T(3) was used as 100%, and the activities with 3,3'-T(2), rT(3), T(4), and 3,5-diiodothyronine (3, 5-T(2)) were 614, 314, 25, and 4%, respectively. We report for the first time the characterization of human SULT1C1 with T(3) and the preferences of the enzyme for various iodothyronines. The presence of SULT1C1 in the adult thyroid gland raises the possibilities that the enzyme can contribute to intraglandular thyroid hormone processing and iodide reutilization.     

Phenotype of the Cyp1a1/1a2/1b1-/- triple-knockout mouse

Crossing the Cyp1a1/1a2(-/-) double-knockout mouse with the Cyp1b1(-/-) single-knockout mouse, we generated the Cyp1a1/1a2/1b1(-/-) triple-knockout mouse. In this triple-knockout mouse, statistically significant phenotypes (with incomplete penetrance) included slower weight gain and greater risk of embryolethality before gestational day 11, hydrocephalus, hermaphroditism, and cystic ovaries. Oral benzo[a]pyrene (BaP) daily for 18 days in the Cyp1a1/1a2(-/-) produced the same degree of marked immunosuppression as seen in the Cyp1a1(-/-) mouse; we believe this reflects the absence of intestinal CYP1A1. Oral BaP-treated Cyp1a1/1a2/1b1(-/-) mice showed the same "rescued" response as that seen in the Cyp1a1/1b1(-/-) mouse; we believe this reflects the absence of CYP1B1 in immune tissues. Urinary metabolite profiles were dramatically different between untreated triple-knockout and wild-type; principal components analysis showed that the shifts in urinary metabolite patterns in oral BaP-treated triple-knockout and wild-type mice were also strikingly different. Liver microarray cDNA differential expression (comparing triple-knockout with wild-type) revealed at least 89 genes up- and 62 genes down-regulated (P-value < or = 0.00086). Gene Ontology "classes of genes" most perturbed in the untreated triple-knockout (compared with wild-type) include lipid, steroid, and cholesterol biosynthesis and metabolism; nucleosome and chromatin assembly; carboxylic and organic acid metabolism; metal-ion binding; and ion homeostasis. In the triple-knockout compared with the wild-type mice, response to zymosan-induced peritonitis was strikingly exaggerated, which may well reflect down-regulation of Socs2 expression. If a single common molecular pathway is responsible for all of these phenotypes, we suggest that functional effects of the loss of all three Cyp1 genes could be explained by perturbations in CYP1-mediated eicosanoid production, catabolism and activities.     

间质作用因子1通过正调控窖蛋白1抑制FBJ-S1-H的迁移性

目的证明间质作用因子(stromal interaction molecule1,Stim1)在FBJ诱导的小鼠骨肉瘤细胞中的抑癌作用。方法在Stim1高表达的FBJ-S1-H细胞采用Stim1以siRNA干扰技术得到Stim1沉默的几株S1-H单克隆细胞株,通过细胞行为学方法和RT-PCR技术对其mRNA进行研究,通过明胶酶谱法对细胞基质金属酶活性进行研究。结果通过细胞行为学方法证明,Stim1的沉默提高了细胞的迁移性,通过对mRNA表达的研究发现,Stim1沉默引起了多种基因表达的变化,其中包括基质金属酶9(matrix mexalloprotelnase 9,MMP-9)的升高,窖蛋白(caveolinl,Cav1),甾醇调控因子Srebf1的降低等,提高单克隆细胞中的Cav1含量可以使细胞迁移性降低。结论实验结果证明在FBJ-S1-H细胞中,Stim1能够抑制细胞的移动性,沉默Stim1的表达能够提高细胞的迁移性。