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Objective Visfatin is a newly identified adipocytokine and recent studies indicated that visfatin may have potential proinflammatory effect. However, its pathophysiological role in the metabolic syndrome (MetS) is not fully understood. In this study we investigated whether serum visfatin levels is altered in patients with the MetS, and compared the levels of visfatin between patients with and without carotid plaques. Design and method A total of 139 patients with MetS and 105 controls were included. The patients were further divided into two groups: 40 with carotid plaques and 99 without carotid plaques. Serum visfatin was measured by using enzyme immunoassay method and carotid intimal-media thickness (IMT) was measured by ultrasound in all subjects. Results Serum visfatin was elevated in both MetS patients with and without carotid plaques compared to controls (log visfatin: 1·14 ± 0·14 vs. 0·99 ± 0·17 ng/ml vs. 0·93 ± 0·23 ng/ml, P < 0·001 and P < 0·05 vs. control group, respectively), and in patients with carotid plaques more than in patients without carotid plaques ( P < 0·001). Multiple stepwise regression analysis revealed that only LDL-cholesterol correlated with visfatin, and visfatin independently correlated with max IMT in the patients with MetS. A log visfatin > 1·08 ng/ml had 70% sensitivity and 67% specificity for detecting patients with carotid plaques. Conclusions/interpretation Our results showed that serum visfatin was increased in patients with MetS, especially in those with carotid plaques. Visfatin may be an inflammatory marker of MetS. [ABSTRACT FROM AUTHOR]

An efficient micellar electrokinetic capillary chromatography method was developed to analyze three major active components including morroniside, loganin and gallic acid in Fructus corni and its six preparations for the first time. The factors that could affect the separation were studied, such as the pH of the buffer, concentrations of SDS, organic modifier and β-CD, and the applied voltage. The optimum analysis conditions were 10 mmol/L NaH2PO4–5 mmol/L Na2B4O7 (pH 6.8) buffer containing 140 mmol/L SDS, 1 mmol/L β-CD, 5% (v/v) methanol and 12.5 kV applied voltage. The linearity between the peak-areas and the concentrations of the analytes were investigated, and they exhibit excellent linear behavior over the concentration ranges (correlation coefficients 0.9953–0.9995). In addition, the pKa of gallic acid was determined using capillary zone electrophoresis. The result was consistent with that reported by the literature. Copyright © 2003 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

In this study, MJ-29(6-pyrrolidinyl-2-(2-substituted phenyl)-4-quinazolinones derivatives) was examined for its growth inhibition effect on U937 human leukemia cell line. After 24 hours treatment of MJ-29,PI incorporation was applied to determine the proliferation rate. A dose and time-dependent decrease in cell proliferation was observed. The cytotoxic effect of MJ-29 on normal cells (HUVEC and peripheral mononuclear cells) was lower than that on U937 cells of treatment. Cell cycle analysis of U937 cells showed that MJ-29 induced significant G2/M arrest and apoptosis. Immuno-fluorescence microscopy and in vitro tubulin assembly assays indicated that MJ-29 binding to tubulin and disrupts microtubule organization. We found that MJ-29 up-regulated the protein levels of p161-CDK1,Chk1,Chk2,p21 and increased cyclin B and CDK1 kinase activity. MJ-29-treated U937 cells presented typical apoptosis by DAPI staining, increase of Annexin V binding, internucleosomal DNA cleavage. In addition, release of cytosolic cytochrome c¡BPro-caspase-9¡BApaf-1 and AIF, down-regulation of Bcl-2, Bcl-xL¡B xIAP¡BclAP-1¡BclAP-2 and up-regulation of phospho-Bcl-2¡BBax¡BBad¡BBak were detected by western blotting. Caspases activity assay and Sub-G1 nuclei analysis of MJ-29-treated U937 indicated that the MJ-29 induced apoptosis was mainly mediated by activation of caspase 9 and 3. Our results indicated that the ability of MJ-29 to inhibit cell proliferation may be mediated by both the induction of mitotic arrest and apoptosis. µ [ABSTRACT FROM AUTHOR]