Selenocystine induces oxidative-mediated DNA damage via impairing homologous recombination repair of DNA double-strand breaks in human hepatoma cells.

Selenocystine (SeC) has been identified as a novel compound with broad-spectrum anticancer activity. However, the effects of SeC on modifying DNA repair mechanism were less addressed. In this study, we demonstrated that SeC selectively induced cytotoxicity and genotoxicity against HepG2 hepatoma cell line. Comet assay revealed SeC-induced DNA damage in HepG2 cells, particularly in the form of DNA double strand breaks (DSBs), corroborated by the increase expression of the DSB marker, gamma-H2AX. We further demonstrated that SeC suppressed DNA homologous recombination repair, exacerbating DNA damage accumulation. Such effects on DNA damage and cell viability inhibition were alleviated by antioxidants, glutathione and Trolox, suggesting the involvement of reactive oxygen species (ROS). High levels of intracellular and mitochondrial ROS were detected in SeC-treated HepG2. In addition, SeC impaired the expression of antioxidant enzymes (superoxidase mutases and catalase), prompting the imbalance between antioxidant protection and excessive ROS formation and eliciting DSBs and cellular death. Decreased procaspase-3, 7, and 9 and Bcl-2 proteins and an increased Bax/Bcl-2 ratio, were observed after SeC treatment, but could be reversed by Torlox, confirming the action of SeC on ROS-induced apoptosis. In vivo, the xenograft tumor model of HepG2 cells validated the inhibition of SeC on tumor growth, and the induction of DSBs and apoptosis. In summary, SeC has the capability to induce ROS-dependent DNA damage and impeded DBS repair in HepG2 cells. Thus, SeC holds great promise as a therapeutic or adjuvant agent targeting DNA repair for cancer treatment.

One-kilojoule pulsed-power generator for laboratory space sciences.

This paper reports on the assembly of a compact, low-cost, pulsed-power facility used for plasma studies. The construction uses two modules placed on opposite sides of the test chamber to minimize the system impedance and improve access to test samples. The stored energy is 1  kJ with a peak current of 135  kA and a 1592  ns quarter-period time. Up until now, an imploding conical-wire array has been studied by using time-integrated (visible) imaging, and time-resolved laser imaging, providing a measure of the plasma jet speed in the range of 170  km/s. Our future plans will continue to investigate high-energy-density plasmas that are relevant to the space environment, fusion, and spectroscopy.

Rail-gap switch with a multistep high-voltage triggering system.

A rail-gap switch with a multistep triggering system was developed. The rail-gap switch consisted of two rail-like electrodes and a knife-edge electrode parallel to each other. It was assembled from many pieces and filled with unpressurized-flowing dry air. Good alignments between all electrodes were achieved by using a special jig and the knife-edge electrode as the spatial reference. Furthermore, to trigger the rail-gap switch, a multistep triggering system was used. The triggering system consisted of three components: an optical trigger-pulse generator, a slow high-voltage trigger-pulse generator using an ignition coil for a car, and finally, a fast high-voltage trigger-pulse generator using a three-stage Marx generator. The triggering system generated a negative high-voltage trigger pulse of less than -40 kV with a falling speed of -6.6 ± 0.4 kV/ns. The falling speed was fast enough to initiate multichannel discharges in the rail-gap switch. Finally, the rail-gap switch was tested using a test bench consisting of a 0.5-µF capacitor bank charged to 20 kV. The rail-gap switch was triggered by the multistep triggering system robustly with a delay of 180 ns. The delay between the time, when the peak current of the test bench occurred, and the trigger pulse was 890 ns with a jitter of 20 ns, i.e., ∼2% uncertainty in time. The inductance of the rail-gap switch was ∼80 nH obtained from the discharge tests. The rail-gap switch with the multistep high-voltage triggering system is suitable for any pulsed-power systems with current rise times in the order of 1 µs.

Liraglutide downregulates hepatic LDL receptor and PCSK9 expression in HepG2 cells and db/db mice through a HNF-1a dependent mechanism.

BACKGROUND: Proprotein convertase subtilisin/kexin type 9 (PCSK9), a major regulator of cholesterol homeostasis, is associated with glucose metabolism. Liraglutide, a glucagon-like peptide-1 receptor agonist, can increase insulin secretion in a glucose-dependent manner and lower blood glucose. We aimed to investigate the relationship between liraglutide and PCSK9. METHODS: At the cellular level, the expressions of PCSK9 and hepatocyte nuclear factor 1 alpha (HNF1α) protein in HepG2 cells stimulated by liraglutide was examined using Western blot. Seven-week old db/db mice and wild type (WT) mice were administered either liraglutide (200 µg/kg) or equivoluminal saline subcutaneously, twice daily for 7 weeks. Fasting glucose level, food intake and body weight were measured every week. After the 7-week treatment, the blood was collected for lipid and PCSK9 levels detection and the liver was removed from the mice for oil red O staining, immunohistochemical analysis, immunofluorescence test and Western bolt. RESULTS: Firstly, liraglutide suppressed both PCSK9 and HNF1α expression in HepG2 cells in a time and concentration dependent manner. Secondly, liraglutide induced weight loss in WT and db/db mice, decreased serum PCSK9, glucose and lipid levels and improved hepatic accumulation in db/db but not WT mice. Thirdly, liraglutide reduced both hepatic PCSK9 and low-density lipoprotein receptor (LDLR) expression with a decrease in HNF1α in db/db mice but not in WT mice. CONCLUSIONS: Liraglutide suppressed PCSK9 expression through HNF1α-dependent mechanism in HepG2 cells and db/db mice, and decreased LDLR possibly via PCSK9-independent pathways in db/db mice.

Increased Serum Leptin Levels in New-Onset, Untreated Female Patients with Coronary Artery Disease and Positively Associated with Inflammatory Markers.

BACKGROUND/AIMS: Previous studies have suggested that leptin was associated with atherosclerosis and involved in inflammation. Gender differences between leptin and inflammatory markers have been evaluated less in untreated patients with stable coronary artery disease (CAD). METHODS: In this study, a total of 394 consecutive Chinese patients who received coronary artery angiography were enrolled, including 243 patients with CAD and 151 non-CAD controls. The baseline clinical characteristics were collected and serum leptin levels were determined using ELISA. RESULTS: The relation of serum leptin levels to inflammatory markers was found only in female patients. Leptin and white blood cell count (WBCC) as well as its subsets were significantly higher in female patients than female controls. In female patients, leptin was positively associated with C-reactive protein (CRP; r = 0.28, p = 0.016), WBCC (r = 0.261, p = 0.02), neutrophil, r = 0.268, p = 0.018, and monocyte, r = 0.228, p = 0.044. Multivariable regression analysis revealed that leptin was significantly and independently associated with CRP (ß = 0.317, p = 0.004), WBCC (ß = 0.278, p = 0.020), neutrophil (ß = 0.262, p = 0.032), and monocyte (ß = 0.245, p = 0.032). CONCLUSIONS: The serum leptin levels were higher in female patients and independently associated with CRP, WBCC, and its subsets, suggesting a potential interaction between leptin and inflammation in female CAD patients.

Triglyceride to High-Density Lipoprotein Cholesterol Ratio and Cardiovascular Events in Diabetics With Coronary Artery Disease.

BACKGROUND: It has been demonstrated that an elevated ratio of triglycerides (TG) to high-density lipoprotein cholesterol (HDL-C) is a risk factor of coronary artery disease (CAD) in patients with type 2 diabetes mellitus (T2DM) and is also found to be associated with cardiovascular events (CVEs) in the general population. However, its prognostic value in patients with T2DM along with CAD remains to be determined. MATERIALS AND METHODS: A total of 1,447 consecutive patients with T2DM with angiographic-proven stable CAD were enrolled in the present study and followed-up for an average of 20.3 months. The characteristics of all patients including fasting lipid profile were obtained at baseline and multivariate Cox proportional hazards models were constructed using log TG/HDL-C as a predictor variable. The relationships between CVEs and total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), non-HDL-C, TC/HDL-C, LDL-C/HDL-C and apolipoprotein B/ apolipoprotein AI (apoB/apoAI) were also explored. RESULTS: Compared with patients without CVEs, the ones who experienced CVEs had a higher TG/HDL-C ratio. Univariable regression revealed a significant association of log TG/HDL-C with CVEs (hazard ratio = 2.5, P = 0.015). After adjusting for multiple traditional risk factors of cardiovascular disease, the association was still found (hazard ratio = 2.47, P = 0.047). Moreover, results suggested that the ratios of non-HDL-C, TC/HDL-C, LDL-C/HDL-C and apoB/apoAI were not predictors for CVEs in T2DM. CONCLUSIONS: In our primary study, data suggested that elevated TG/HDL-C value might be a useful predictor for future CVEs in Chinese patients with T2DM with stable CAD. Further study is needed to confirm our findings.

Serum fibrinogen and cardiovascular events in Chinese patients with type 2 diabetes and stable coronary artery disease: a prospective observational study.

OBJECTIVES: The aim of this study was to investigate the association of serum fibrinogen with cardiovascular events (CVE) in Chinese patients with type 2 diabetes mellitus (T2DM) and stable coronary artery disease (CAD). DESIGN: An observational study. SETTING: FuWai Hospital in Beijing, China. PARTICIPANTS: A cohort of 1466 patients with T2DM and angiographic-proven stable CAD was evaluated. OUTCOME MEASURES: Baseline serum fibrinogen levels were measured and trisected into 'low', 'middle' and 'high'. Their association with CVE was explored using Cox proportional hazard models. RESULTS: With 20.2 months (average) follow-up, 44 (3%) were lost to follow-up and 96 patients developed CVE. Compared with the patients without CVE, the ones who developed CVE had higher levels of fibrinogen. Univariable regression revealed a significant relation of fibrinogen to CVE (HR (HR) 1.25, 95% CI 1.06 to 1.47, p=0.010) per SD increase of fibrinogen at baseline. After adjusting for multiple established cardiovascular disease (CVD) risk factors, the association persisted (HR 1.30, 95% CI 1.02 to 1.66, p=0.037). Moreover, after adjusting for CVD risk factors, the HRs for middle-serum and high-serum fibrinogen concentration, using 'low' group as reference, were 1.23 (95% CI 0.69 to 2.20) and 2.20 (95% CI 1.11 to 3.36, p=0.049). CONCLUSIONS: We first indicated that elevated fibrinogen level was independently associated with increased CVE in Chinese patients with T2DMand stable CAD.

Relationship of lipid and lipoprotein ratios with coronary severity in patients with new on-set coronary artery disease complicated with type 2 diabetics.

BACKGROUND: Diabetes mellitus (DM) is associated with coronary artery disease (CAD) progression. Although previous studies have demonstrated the association of lipid and lipoprotein ratios with CAD, no data are currently available concerning the relationship between lipid and lipoprotein ratios and the severity of new on-set CAD in diabetics. Therefore, the aim of the present study was to investigate the usefulness of lipid and lipoprotein ratios in predicting the severity of CAD in patients with type 2 DM (T2DM). METHODS: A total of 380 consecutive T2DM patients with new on-set CAD were enrolled in the present study. Then, they were classified into the three groups according to Gensini score (GS) tertiles. The relationship between lipid and lipoprotein ratios currently used and the GS was investigated. RESULTS: Positive correlations of natural log-transformed GS (lnGS) with apolipoprotein B to apoA-I ratio (apoB/apoA-I), non-high-density lipoprotein cholesterol to apoA-I ratio (non-HDL-C/apoA-I), and low-density lipoprotein cholesterol to apoA-I ratio (LDL-C/apoA-I) were found (r = 0.18, 0.13, 0.12, respectively, all P < 0.05). Multivariate logistic analysis indicated apoB/apoA-I as the strongest predictor for high GS (OR = 5.67, 95% CI: 1.45-23.92, P = 0.003). Area under receivers operating characteristic curve of apoB/apoA-I was 0.63 (95% CI: 0.60-0.66, P = 0.001) for predicting high GS. The optimal cutoff value of apoB/apoA-I to predict high GS was 0.72 with the sensitivity of 61.2% and the specificity of 62.1%. CONCLUSIONS: Lipid and lipoprotein ratios might be useful for predicting the severity of new on-set CAD in T2DM patients, and the apoB/apoA-I appeared as the most significant predictor in this population.

Circulating MicroRNAs as Novel Diagnostic Biomarkers for Very Early-onset (≤40 years) Coronary Artery Disease.

OBJECTIVE: Very early-onset coronary artery disease (CAD) is a great challenge in cardiovascular medicine throughout the world, especially regarding its early diagnosis. This study explored whether circulating microRNAs (miRNAs) could be used as potential biomarkers for patients with very early-onset CAD. METHODS: We performed an initial screening of miRNA expression using RNA isolated from 20 patients with angiographically documented very early-onset CAD and 20 age- and sex-matched normal controls. For further confirmation, we prospectively examined the miRNAs selected from 40 patients with very early-onset CAD and 40 angiography-normal controls. RESULTS: A total of 22 overexpressed miRNAs and 22 underexpressed miRNAs were detected in the initial screening. RT-qPCR analysis of the miRNAs obtained from the initial screening revealed that four miRNAs including miR-196-5p, miR-3163-3p, miR-145-3p, and miR-190a-5p exhibited significantly decreased expression in patients compared with that in controls (P<0.05). The areas under the receiver operating characteristic curve for these miRNAs were 0.824 (95% CI, 0.731-0.917; P<0.001), 0.758 (95% CI, 0.651-0.864; P<0.001), 0.753 (95% CI, 0.643-0.863; P<0.001), and 0.782 (95% CI, 0.680-0.884; P<0.001), respectively, in the validation set. CONCLUSION: To our knowledge, this is an advanced study to report about four serum miRNAs (miR-196-5p, miR-3163-3p, miR-145-3p, and miR-190a-5p) that could be used as novel biomarkers for the diagnosis of very early-onset CAD.

Leptin decreases the expression of low-density lipoprotein receptor via PCSK9 pathway: linking dyslipidemia with obesity.

BACKGROUND: Previous studies have suggested that people with obesity showed elevated serum levels of leptin as well as lipid dysfunction and proprotein convertase subtilisin/kexin type 9 (PCSK9) played an important role in the regulation of lipid metabolism recently. The aim of this study was to determine if leptin participated in regulating the uptake of low-density lipoproteins (LDL) in hepatocytes via PCSK9. METHODS: HepG2 cells were treated with human recombinant leptin. The impact of leptin on cellular low density lipoprotein receptor (LDLR) and PCSK9 protein levels was determined by Western blot. Dil-LDL uptake assay was performed to examine the LDLR function. Specific small interfering RNAs (siRNAs) were used to interfere the expressions of target proteins. RESULTS: The expression of LDLR and LDL uptake could be significantly down-regulated by leptin treatment while the expressions of PCSK9 and hepatocyte nuclear factor 1α (HNF1α) were enhanced in HepG2 cells. Furthermore, inhibition of PCSK9 or HNF1α expression by siRNAs rescued the reduction of LDLR expression and LDL uptake by leptin. We found that leptin activated the p38 mitogen-activated protein kinase (p38MAPK) signaling pathway. Moreover, the changes of the expressions of HNF1α, PCSK9, LDLR, and LDL uptake induced by leptin could be blocked by p38MAPK inhibitor (SB203580). Additionally, leptin attenuated the up-regulation of LDLR caused by atorvastatin in HepG2 cells. CONCLUSIONS: These findings indicated firstly that leptin reduced LDLR levels in hepatocyte via PCSK9 pathway, suggesting that PCSK9 might be a alternative target for dyslipidemia in the obesity.

Plasma PCSK9 level is unrelated to blood pressure and not associated independently with carotid intima-media thickness in hypertensives.

Proprotein convertase subtilisin/kexin type 9 (PCSK9), a novel target for low-density lipoprotein cholesterol (LDL-C)-lowering therapy, has been found to possess multiple off-target effects in humans. The aim of the present study was to investigate the association of blood pressure (BP) with plasma PCSK9 levels in a large Chinese cohort and the relation of PCSK9 level to carotid intima-media thickness (cIMT) in hypertensive patients. A total of 805 patients without lipid-lowering drug therapy were consecutively enrolled. First, the relationship between BP and PCSK9 was evaluated in hypertensives and normotensives. Furthermore, we examined the relation of PCSK9 to cIMT in 256 enrolled patients who had received a carotid ultrasound test. Plasma PCSK9 levels were measured by enzyme-linked immunosorbent assay, and cITM of left and right carotid arteries was assessed by B-mode ultrasound. There was no significant difference in PCSK9 levels between hypertensives and normotensives. PCSK9 level was not associated with systolic and diastolic BP and pulse pressure in hypertensives and normotensives regardless of sex. A positive correlation between PCSK9 and maximum-IMT and mean-MIT in hypertensives was found in univariate analyses, whereas such an association was absent in normotensives. In addition, the positive association of PCSK9 with cIMT disappeared in hypertensives in multivariate analyses. PCSK9 level is not associated with systolic or diastolic BP in hypertensives or normotensives, but it positively correlates with cIMT in hypertensives in univariate but not multivariate analyses, and further researches are needed.

ABO blood group system and the coronary artery disease: an updated systematic review and meta-analysis.

ABO blood group system, a well-known genetic risk factor, has clinically been demonstrated to be linked with thrombotic vascular diseases. However, the relationship between ABO blood group and coronary artery disease (CAD) is still controversial. We here performed an updated meta-analysis of the related studies and tried to elucidate the potential role of ABO blood group as a risk factor for CAD. All detectable case-control and cohort studies comparing the risk of CAD in different ABO blood groups were collected for this analysis through searching PubMed, Embase, and the Cochrane Library. Ultimately, 17 studies covering 225,810 participants were included. The combined results showed that the risk of CAD was significantly higher in blood group A (OR = 1.14, 95% CI = 1.03 to 1.26, p = 0.01) and lower in blood group O (OR = 0.85, 95% CI = 0.78 to 0.94, p = 0.0008). Even when studies merely about myocardial infarction (MI) were removed, the risk of CAD was still significantly higher in blood group A (OR = 1.05, 95% CI = 1.00 to 1.10, p = 0.03) and lower in blood group O (OR = 0.89, 95% CI = 0.85 to 0.93, p < 0.00001). This updated systematic review and meta-analysis indicated that both blood group A and non-O were the risk factors of CAD.

Plasma d-Dimer as a Useful Marker Predicts Severity of Atherosclerotic Lesion and Short-Term Outcome in Patients With Coronary Artery Disease.

Increased d-dimer is indicative of a hypercoagulable state and found to be associated with acute coronary syndromes. The present study aimed to evaluate whether plasma d-dimer levels could predict subsequent major clinical events in patients with coronary artery disease (CAD). First, 2209 angiographic-proven patients with CAD were consecutively enrolled. Then, all patients were subjected to follow up for an average of 18 months (ranged from 14 to 1037 days). The relationships of the plasma d-dimer with the severity of CAD and future clinical outcomes were evaluated. We found that plasma d-dimer was higher in patients with prior myocardial infarction (MI) than that in patients with nonprior MI (P = .006). Multivariate linear regression analysis suggested that the plasma d-dimer was linked to the severity of CAD assessed by Gensini score (ß = 0.052, 95% confidence interval [CI]: 1.20-6.84, P = .005) even after adjusting for confounding factors. During the follow-up, 42 patients underwent prespecified outcomes. After adjustment for multiple variables in the Cox regression model, the d-dimer levels remained to be a potential predictor of total outcome (hazard ratio = 1.22, 95% CI: 1.09-1.37, P = .001). Therefore, plasma d-dimer levels appeared to be a useful predictor for the severity of CAD and the subsequent major clinical events.

Positive correlation of plasma PCSK9 levels with HbA1c in patients with type 2 diabetes.

BACKGROUND: Proprotein convertase subtilisin/kexin type 9 (PCSK9) has been demonstrated to be involved in not only lipid metabolism but also glucose homeostasis. Glycated haemoglobin (HbA1c ) is a 'gold standard' for monitoring long-term glycaemic control. However, the correlation of plasma PCSK9 levels with HbA1c remains undetermined. METHODS: We consecutively enrolled 805 subjects undergoing coronary angiography, including 176 patients with type 2 diabetes mellitus (T2DM) and 629 non-diabetic patients. The baseline characteristics were collected, and serum PCSK9 level was assessed by ELISA. Univariable regression analysis and multiple-variable regression analysis were used to examine the associations of PCSK9 with HbA1c . Furthermore, the HbA1c was compared across the tertiles of PCSK9 levels. And also, PCSK9 levels were compared in poorly controlled (HbA1c ≥ 7.0%) and well-controlled (HbA1c < 7.0%) patients with T2DM. RESULTS: PCSK9 levels were positively correlated with low-density lipoprotein cholesterol in both T2DM and non-T2DM. Univariable regression analysis revealed a positive association between PCSK9 and HbA1c in patients with T2DM (ß = 0.255, p = 0.001) but not in patients without diabetes (ß = 0.061, p = 0.128). Multiple-variable regression analysis exhibited that PCSK9 was independently correlated with HbA1c in T2DM after adjustment for traditional atherosclerotic risk factors (ß = 0.197, p = 0.020). Moreover, HbA1c level was higher in patients with the highest tertile of PCSK9 than that in the lowest tertile (p = 0.042). Additionally, higher levels of PCSK9 were found in poorly controlled group compared with the well-controlled group (p = 0.029). CONCLUSIONS: Data suggest a positive correlation of PCSK9 levels with HbA1c in patients with T2DM but not in patients without T2DM, indicating a potential role of PCSK9 in T2DM. Copyright © 2015 John Wiley & Sons, Ltd.

Pharmacokinetics of silybin nanoparticles in mice bearing SKOV-3 human ovarian carcinoma xenocraft.

The particle fabrication technique was used to fabricate monodisperse size and shape specific poly (lactide-co-glycolide) particles loaded with the silybin. Response surface methodology (RSM) using the central composite rotatable design (CCRD) model was used to optimize formulations of silybin nanoparticles. Further the optimized nanoparticles are characterized for particle size, zeta potential, surface morphology, entrapment efficiency, in-vitro drug release, silybin availability for tumor, plasma, lung, spleen, liver were determined. The significant findings were the optimal formulation of PLGA concentration 10 mg, PVA concentration 2000 and PET width of 6 gave rise to the EE of 88%, mean diameter of 223 nm and zeta potential of 25-mV. Release studies were investigated at pH 1.2 and pH 6.8. It was studied that lower the pH, faster the release of sylibin. The nanoparticles had~15-fold higher plasma exposure as measured by AUC contrasted to pure silybin. The nanoparticles had a 60% increase altogether tumor silybin presentation contrasted with pure silybin. Nanoparticles had higher silybin presentation in the spleen and liver contrasted with pure silybin suspension as expected for a nanoparticle formulation. The lung silybin presentation for the nanoparticle was additionally 2-fold higher than that of the pure silybin suspension. The results of pharmacokinetic parameters and oral bioavailability data exhibited that drug-nanoparticle complex could enhance the oral absorption of silybin and as well as the use of particles with smaller feature size may be preferred to decrease clearance by organs of the mononuclear phagocyte system.

Oxidized low-density lipoprotein-induced CD147 expression and its inhibition by high-density lipoprotein on platelets in vitro.

INTRODUCTION: Matrix metalloproteinases (MMPs) are believed to progressively degrade the collagenous components of the protective fibrous cap, leading to atherosclerotic plaque rupture or destabilization. Oxidized low-density lipoprotein (ox-LDL) enhances the release of CD147, known as the extracellular MMP inducer, from coronary smooth muscle cells. However, whether ox-LDL can induce platelet CD147 expression is unknown. Therefore, we investigated the influence of ox-LDL and high-density lipoprotein (HDL) on CD147 expression on human platelets. MATERIALS AND METHODS: Washed platelets were incubated with ox-LDL (or native LDL) and HDL or anti-LOX-1 monoclonal antibody prior to incubation with ox-LDL. In parallel, buffer (PBS) was added to washed platelets as a control. The expression levels of CD147, CD62P, CD63 and Annexin V were assessed by flow cytometry, and soluble CD147 from the platelets was assessed by an enzyme-linked immunosorbent assay. Laser scanning microscopy (LSM) and transmission electron microscopy (TEM) were used to visualize the morphological changes and granule release, respectively, from the platelets. RESULTS: Platelets treated with ox-LDL exhibited a significant increase in the expression of CD147 (or Annexin V), followed by increases in CD62P and CD63, compared with the control group. In contrast, HDL or anti-LOX-1 monoclonal antibody decreased these effects. The expression of soluble CD147 increased as the concentration of ox-LDL used to treat the platelets increased. After exposure to ox-LDL, morphological changes and granule release in the platelets were visualized by LSM and TEM. Additionally, the TEM revealed that HDL inhibits alpha-granule release. CONCLUSIONS: In platelets, ox-LDL stimulates the release of CD147 via binding to LOX-1, whereas HDL inhibits this effect. This finding could provide new insights concerning the influence of ox-LDL and HDL on plaque stability by the up-regulation of CD147 on platelets.

Determinations of the inclusion complex between gossypol and beta-cyclodextrin.

Features of the inclusion complex between gossypol (Gos) and beta-cyclodextrin (CD), such as its aqueous solubility, association constant, characteristics in the solid state and crystalline morphology, as well as the stoichiometry of this complex have been determined. The phase-solubility diagram drawn using UV detections belongs to an AN-type. Fluorescence detection and calculation with the modified Benesi-Hidebrond equation provide an 1:2 stoichiometry for the complex. Its apparent stability constant has been determined to be 3,203 M(-1) by fluorescence technique and confirmed by the calculation from UV spectroscopy. X-ray powder diffractions (XRD) and Scanning Electron Microscopy (SEM) observations showed a clear difference in the crystal morphology of the complex from those of both Gos and beta-CD.

Study on structure and characterization of inclusion complex of gossypol/beta cyclodextrin.

The inclusion complex of beta-cyclodextrin with gossypol was synthesized by using a convenient method of microwave irradiation. The structure of the complex was determined by 1H NMR, IR spectroscopy, and as well as the elemental analysis; the thermal stability was studied by means of differential thermal analysis (DTA) and thermogravimetric analysis (TGA). The association constant between gossypol and beta-cyclodextrin measured via UV spectroscopy was 4462M(-1) at room temperature, following stoichiometry 1:2.