The contents of gallic acid, catechin, albiflorin, paeoniflorin, benzoic acid and paeonol extracted in different growth years, collecting season and of different parts of Paeonia lactiflora were determined. The results showed that the contents of catechin and paeoniflorin in Paeonia lactiflora collected in autumn are the highest, and the contents of benzoic acid was lower than that of those collected at other time. The longer is the age of Paeonia lactiflora, the higher is the contents of catechin and paeoniflorin. The contents of catechin and paeoniflorin in the root of Paeonia lactiflora were higher than those in other parts of the plant. There is a certain content of paeoniflorin in the leaves of Paeonia lactiflora. Judging from the result, paeoniflorin is synthesized in the leaf and then transported to the root. Catechin is not synthesized in the leaf, but mainly in the root. Paeonia lactiflora should be collected in autumn, and immature plant should not be collected.
Acetophenones ; analysis ; Benzoates ; analysis ; Benzoic Acid ; analysis ; Bridged-Ring Compounds ; analysis ; Catechin ; analysis ; Chromatography, High Pressure Liquid ; methods ; Drugs, Chinese Herbal ; analysis ; Gallic Acid ; analysis ; Glucosides ; analysis ; Monoterpenes ; Paeonia ; chemistry ; Plant Leaves ; chemistry ; Plant Roots ; chemistry ; Plants, Medicinal ; chemistry ; Seasons

OBJECTIVETo develop a simple and rapid capillary electrophoresis (CE) method for the separation and determination of four active organic acids including salicylic acid, syringic acid, benzoic acid, and anthranilic acid in Radix Isatidis.

METHODThe HPCE system consisted of a fused-silica capillary column of 47.3 cm (38.3 cm to the detector) x50 microm i.d. and a mixture ofacetonitrile-borate buffer (15% acetonitrile, 25 mmol L(-1) borate, 15 mmol L(-1) beta-CD, pH 9.10) solution as the operating buffer. The applied voltage was 11.5 kV and the UV detection was set at 220 nm. The effects of the applied voltage, detection wavelength, and the pH of buffer, the concentration of buffer, acetonitrile and beta-CD were investigated.

RESULTThe linear calibration rang was 3.0-90 mg L(-1) (r=0.9994) for salylic acid, 4.0-120 mg L(-1) (r=0.9995) for syringic acid, 2.0-60 mg L(-1) (r=0.9998) for benzoic acid and 5.0-100 mg L(-1) (r=0.9992) for anthranilic acid. The recoveries of salylic acid, syringic acid, benzoic acid and anthranilic acid were 95.9%-102.6%, 98.6%-103.4%, 98.7%-104.1%, 96.1%-104.3% respectively. The detection limits of salylic acid, syringic acid, benzoic acid and anthranilic acid were 0.7, 1.1, 1.2 and 1.5 mg L(-1), respectively.

Benzoic Acid ; analysis ; Electrophoresis, Capillary ; Gallic Acid ; analogs & derivatives ; analysis ; Isatis ; chemistry ; Linear Models ; Reproducibility of Results ; Salicylic Acid ; analysis ; Sensitivity and Specificity ; ortho-Aminobenzoates ; analysis

No abstract available.
Benzamides ; Mesylates* ; Nails, Malformed* ; Piperazines ; Pyrimidines ; Imatinib Mesylate

No abstract available.
Benzamides ; Drug Eruptions* ; Mesylates* ; Piperazines ; Pyrimidines ; Imatinib Mesylate

Benzoates ; urine ; Gas Chromatography-Mass Spectrometry ; methods ; Humans

Blood eosinophilia can be classified as either familial or acquired. Familial eosinophilia is a rare autosomal dominant disorder characterized by a stable eosinophil count. Acquired eosinophilia is classified further into a primary or secondary phenomenon depending on whether eosinophils are considered integral to the underlying disease. Primary eosinophilia is considered clonal in the presence of either a cytogenetic abnormality or bone marrow histological evidence of classified hematologic malignancies. Causes of secondary eosinophilia include infections, allergic or immunologic disorders, and drugs. Idiopathic eosinophilia belongs to a category of primary eosinophilia, and this is a diagnosis of exclusion. Cases with eosinophilia that lack evidence of clonality may be diagnosed as idiopathic hypereosinophilic syndrome after all causes of reactive eosinophilia have been eliminated. Genetic mutations involving the platelet-derived growth receptor genes (PDGFRA and PDGFRB) have been pathogenetically linked to clonal eosinophilia, and their presence predicts the treatment response to imatinib. In this review, I will present a clinical summary of both familial and acquired eosinophilia with emphasis on recent developments in molecular pathogenesis and treatment.
Benzamides ; Bone Marrow ; Chromosome Aberrations ; Eosinophilia ; Eosinophils ; Hematologic Neoplasms ; Hypereosinophilic Syndrome ; Piperazines ; Pyrimidines ; Imatinib Mesylate

Gastrointestinal stromal tumor (GIST) is a relatively rare disease accounted for less than 1% of gastrointestinal tumors. In the past, surgery is the only reliable therapy for the locoregional GISTs. But with the development of the specific target agents such as imatinib or sunitinib, advanced metastatic GIST can be cured now. GISTs are incidentally found by endoscopic ultrasound or laparoscopic surgery for the abdominal mass and positive immunostain for KIT with characteristic histopathology is mandatory for the diagnosis. Mutational analyses for KIT and PDGFRA is helpful in the diagnosis and treatment of GISTs. Because most GISTs are potentially malignant and surgery itself has high recurrence rate, it should be treated at an early stage and chemotherapy should be considered aggressively. The tumor size, mitotic index, and the involved organs are important prognostic factors. In this paper, the pathogenesis of histopathology, clinical diagnosis and treatment of GISTs were reviewed.
Benzamides ; Gastrointestinal Stromal Tumors ; Indoles ; Laparoscopy ; Mitotic Index ; Piperazines ; Pyrimidines ; Pyrroles ; Rare Diseases ; Recurrence ; Imatinib Mesylate

OBJECTIVETo investigate the effect of tyrosine kinase inhibitor ZD6474 (Vandetanib) on the proliferative inhibition of K562 cells and its derived imatinib-resistant K562/G cells and its mechanism.

METHODSImatinib-resistant K562/G cells were obtained by culturing cells in gradually increasing concentrations of imatinib. The changed factors related to drug-resistance were tested by Western blot. ZD6474 and imatinib affected K562/G and parental K562 cells proliferation were analyzed by WST assay. Flow cytometry was used to analyze cell cycle. Direct inhibition of Src activity by ZD6474 was measured by a colorimetric ELISA assay with recombinant human Src kinase.

RESULTS10 µmol/L imatinib failed to inhibit K562/G cells proliferation or induce cell cycle arrest. Compared with that in parental K562 cells, there were marked high levels of p-Src and Src protein in K562/G cells. The expression of Bcl-2 and p-STAT3 also increased in K562/G cells. After 48 hours incubation, the IC(50) values of ZD6474 in K562 and K562/G cells were 1.61 µmol/L and 3.18 µmol/L, respectively. ZD6474 treatment caused accumulation of cells in the G(0)/G(1) fraction and cell apoptosis in K562 and K562/G cells. ZD6474 decreased the expression of p-Src and Src at post-transcriptional level. Moreover, ZD6474 increased the ratio of Bax/Bcl-2 and decreased the expression of p-STAT3 at the same concentration for inducing apoptosis.

CONCLUSIONSZD6474 is effective in inhibiting the proliferation of imatinib-resistant K562/G cells and parental K562 cells, and induces their apoptasis by significant inhibition of Src kinase activity. Our study provides a reliable experimental basis for chronic myeloid leukemia treatment with ZD6474.

Apoptosis ; drug effects ; Benzamides ; pharmacology ; Humans ; Imatinib Mesylate ; K562 Cells ; Piperazines ; pharmacology ; Pyrimidines ; pharmacology

Bladder interstitial cell (IC) is a cell, which lacks thick filaments and dense bodies but with incomplete basement membrane, rough endoplasmic reticulum and golgi apparatus. IC is divided into 4 subtypes: lamina propria IC, intramuscular IC, IC between the detrusor bundles and perivascular IC. There are different ion currents and related activation pathways in the lamina propria IC and intramuscular IC. Ca2+ signaling pathways play an important role in the communication between IC and detrusor. Any bladder lesions affecting the ion current and Ca2+ signaling pathways can lead to bladder dysfunction. The bladder lesions include bladder outlet obstruction, bladder pain syndrome, interstitial cystitis, neurogenic bladder and diabetes. Imatinib mesylate is currently an available treatment target in IC, and electrical stimulation of acupuncture therapy is a new direction.
Benzamides ; Cystitis, Interstitial ; pathology ; Electric Stimulation ; Humans ; Imatinib Mesylate ; Mucous Membrane ; pathology ; Piperazines ; Pyrimidines ; Signal Transduction

BACKGROUND/AIMS: The treatment of chronic myeloid leukemia (CML) has achieved impressive success since the development of the Bcr-Abl tyrosine kinase inhibitor, imatinib mesylate. Nevertheless, resistance to imatinib has been observed, and a substantial number of patients need alternative treatment strategies. METHODS: We have evaluated the effects of deferasirox, an orally active iron chelator, and imatinib on K562 and KU812 human CML cell lines. Imatinib-resistant CML cell lines were created by exposing cells to gradually increasing concentrations of imatinib. RESULTS: Co-treatment of cells with deferasirox and imatinib induced a synergistic dose-dependent inhibition of proliferation of both CML cell lines. Cell cycle analysis showed an accumulation of cells in the subG1 phase. Western blot analysis of apoptotic proteins showed that co-treatment with deferasirox and imatinib induced an increased expression of apoptotic proteins. These tendencies were clearly identified in imatinib-resistant CML cell lines. The results also showed that co-treatment with deferasirox and imatinib reduced the expression of BcrAbl, phosphorylated Bcr-Abl, nuclear factor-kappaB (NF-kappaB) and beta-catenin. CONCLUSIONS: We observed synergistic effects of deferasirox and imatinib on both imatinib-resistant and imatinib-sensitive cell lines. These effects were due to induction of apoptosis and cell cycle arrest by down-regulated expression of NF-kappaB and beta-catenin levels. Based on these results, we suggest that a combination treatment of deferasirox and imatinib could be considered as an alternative treatment option for imatinib-resistant CML.
Antineoplastic Agents/*pharmacology ; Apoptosis/drug effects ; Apoptosis Regulatory Proteins/metabolism ; Benzoates/*pharmacology ; Cell Proliferation/drug effects ; Dose-Response Relationship, Drug ; Drug Resistance, Neoplasm/*drug effects ; G1 Phase Cell Cycle Checkpoints/drug effects ; Humans ; Imatinib Mesylate/*pharmacology ; Iron Chelating Agents/*pharmacology ; K562 Cells ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/*drug therapy/metabolism ; Protein Kinase Inhibitors/*pharmacology ; Signal Transduction/drug effects ; Triazoles/*pharmacology