肾康注射液的薄层鉴别和大黄素含量测定

用薄层色谱法对制剂中大黄、丹参、黄芪进行了定性鉴别,并采用双波长薄层扫描测定了制剂中大黄素的含量。方法简便,结果可靠,重现性好,平均回收率为１００．４％,ＲＳＤ为３．５１％。     

苦参药材中苦参碱含量测定方法比较研究

目的采用高效液相色谱法(HPLC)建立苦参药材中苦参碱含量的测定方法.方法采用配对试验设计,将高效液相色谱法与薄层色谱扫描法(TLCS)测定苦参药材中苦参碱含量进行比较研究,对试验结果进行配对差值均数t检验.结果表明2种方法测定苦参药材中苦参碱含量无差别.结论高效液相色谱法(HPLC)可准确、简便、快速测定苦参药材中苦参碱含量.     

枇杷叶不同炮制品中熊果酸含量的测定

目的了解不同炮制方法的枇杷叶炮制品质量。方法采用双波长扫描法对枇杷叶几种炮制品的熊果酸含量进行测定。结果蜜炙、姜炙(姜汁炒和姜汤煮)的炮制样品中熊果酸含量均高于生品。结论为今后制定合理的炮制工艺提供科学依据。     

薄层扫描法测定金不换药材中延胡索乙素的含量

目的:测定金不换药材中延胡索乙素的含量.方法:采用双波长薄层扫描法(λS=280nm,λR=360nm).结果:延胡索乙素在0.50μg～5.50μg间,点样量与峰面积呈良好线性关系,r=0.9994,回收率为100.33%,RSD=2.46%(n=3).结论:该法精确、简便、重现性好.     

薄层扫描法测定冠心康颗粒中人参皂苷Re含量

目的:建立冠心康颗粒中人参皂苷Re的含量测定方法.方法:采用CamagⅡ薄层扫描仪,硅胶G自制板,氯仿-甲醇-水(65:35:10)10℃以下放置过夜的下层溶液为展开剂,显色剂为10%硫酸乙醇溶液,于105℃烘5 min显色,λs=530 nm,λR=580 nm.结果:人参皂苷Re在0.4～2.0μg范围内,点样量与峰面积呈良好的线性关系,r=0.999 5,平均回收率为98.84%.结论:薄层扫描法简便、准确,可作为冠心康颗粒的质量控制方法.     

薄层扫描法测定染料木素和大豆苷原的含量

目的建立染料木素和大豆苷原的薄层扫描测定方法。方法薄层色谱条件是:吸附剂:聚酰胺-6薄膜,展开剂:苯-丁酮-甲醇(3∶1∶0.5),结果染料木素和大豆苷原均在250nm处有最大吸收,本法线性关系良好(染料木素:r=0.9993;大豆苷原:r=0.9995)。染料木素的平均回收率98.52%(n=5);大豆苷原的平均回收率99.45%(n=5)。结论方法简便,准确,重现性好,可用于测定染料木素和大豆苷原的含量。     

薄层扫描法测定肝得安胶囊中苦参碱的含量

目的：测定肝得安胶囊中苦参碱的含量，方法：硅胶G薄层板，苯－丙酮－醋酸乙酯－浓氨试液（2：3：4：0．2）展开；λs=510nm,λR=650nm。结果：线性范围0．99－4．95μg，平均回收率99．26％，RSD＝3．79％，结论：该方法可用于肝得安胶囊中苦参碱的含量测定。     

癃闭通胶囊中贝母素乙的含量测定

目的:建立癃闭通胶囊中贝母素乙的含量测定方法.方法:双波长薄层扫描法,薄层板:硅胶G-CMC薄层板,展开剂:苯-丙酮-醋酸乙酯-浓氨水(2:3:4:0.2),显色方法:喷以改良碘化铋钾试液.结果:线性范围0.285～2.565μg,平均回收率为98.6%,RSD为2.5%.结论:方法准确、可靠,为控制癃闭通胶囊的质量提供了科学依据.     

Taurolithocholic acid-3 sulfate induces CD95 trafficking and apoptosis in a c-Jun N-terminal kinase-dependent manner

BACKGROUND & AIMS: Prevention of bile acid-induced apoptosis is of therapeutic interest and requires the understanding of underlying mechanisms. METHODS: The effect of tauroursodeoxycholate (TUDC) on taurolithocholic acid-3 sulfate (TLCS)-induced apoptosis was studied in cultured rat hepatocytes. RESULTS: TLCS induced activation of caspases 8, 9, and 3 and hepatocyte apoptosis. These effects were abolished by TUDC in a PI 3-kinase-/protein kinase B (PKB)-, p38(MAPK)-, and extracellular signal-regulated kinase-2 (Erk-2)-independent manner. These protein kinases were activated by both TLCS and TUDC, however, with different kinetics. TLCS, but not TUDC, led to a sustained activation of c-Jun N-terminal kinase (JNK) and CD95 trafficking to the plasma membrane; both TLCS effects were prevented by TUDC. Inhibition of JNK1 or protein kinase C prevented TLCS-induced CD95 membrane trafficking and blunted the apoptotic response. The apoptotic potency of other bile acids paralleled their ability to induce sustained JNK activation. CONCLUSIONS: Protection by TUDC against TLCS-induced apoptosis starts upstream of caspase 8 activation and is independent of a PI 3-kinase-dependent survival pathway. JNK activation may be important for bile acid-induced apoptosis by triggering ligand-independent CD95 surface trafficking and activation of apoptosis.