Objective:To explore influence of probucol combined atorvastatin on blood viscosity ,transcranial Doppler (TCD) indexes and carotid plaque stability in patients with large artery‐derived cerebral infarction .Methods :A total of 100 patients with large artery‐derived cerebral infarction treated in our hospital from Apr 2014 to Apr 2016 were selected .According to random number table ,patients were randomly and equally divided into atorvastatin group (received atorvastatin based on routine treatment ) and combined treatment group (received probucol based on atorv‐astatin group) ,both groups were treated for six months .Related indexes before and after treatment were compared between two groups .Results :Compared with atorvastatin group after treatment ,there were significant reductions in levels of TC ,TG and LDL‐C ,and significant rise in HDL‐C level (P<0.01 all);significant reductions in whole blood high shear viscosity [(6.23 ± 0.38) mPa/s vs .(4.20 ± 0.42) mPa/s] ,whole blood low shear viscosity [(21.17 ± 5.83) mPa/s vs .(18.10 ± 4.44) mPa/s] ,plasma viscosity [ (2.10 ± 0.45) mPa/s vs .(1.72 ± 0.34) mPa/s] and fibrinogen (Fg) level [(4.35 ± 1.36) g/L vs .(3.30 ± 1.38) g/L] ,P<0.01 all;significant rise in systolic blood flow velocity (Vs) [left :(87.43 ± 14.56) cm/s vs .(95.45 ± 18.37) cm/s]and mean blood flow velocity (Vm) [left :(60.89 ± 16.03) cm/s vs .(75.38 ± 19.36) cm/s]of left and right MCA ,significant reduction in pulsatility index(PI) [(0.85 ± 0.22) vs .(0.75 ± 0.12)] , P<0.05 or <0.01;significant reductions in unstable plaque score [(4.93 ± 0.40) scores vs .(4.12 ± 0.35) scores]and recurrence rate of cerebral infarction (16.00% vs .2.00% ) in combined treatment group ,respectiely P=0.001 ,0.014. Conclusion:Probucol combined atorvastatin can significantly reduce blood viscosity ,significantly improve hemodynamics in patients with large artery‐derived cerebral infarction .Its an‐ti‐atherosclerosis effect is obvious ,therefore it can be used to prevent or reduce recurrence of cerebral infarction .

Objective To investigate the correlations of serum cystatin C level with severity of stroke and short-term outcome in patients with acute ischemic stroke.Methods Patients with first-ever acute ischemic stroke aged ≥50 years who did not receive thrombolysis and took a visit within 3 d after onset were selected prospectively.The serum cystatin C level was detected within 24 h after admission and various clinical data were collected.The National Institutes of Health Stroke Scale (NIHSS) was used to assess the neurological deficits on the day of admission.The NIHSS score ＜8 was defined as mild stroke and ≥8 was defined as moderate to severe stroke.The modified Rankin Scale (mRS) was used to evaluate the short-term outcome at discharge or 14 d after onset,0-2 was defined as good outcome and ＞2 was defined as poor outcome.Results A total of 188 patients were enrolled,including 93 (49.5％) females and 95 (50.5％) males,their mean age was 65.4 ±9.2 years old (range 50-87).There were 120 patients with mild stroke (63.8％),68 with moderate to severe stroke (36.2％);106 patients (56.4％) had good outcome and 82 (43.6％) had poor outcome.Univariate analysis showed that serum cystatin C level in the moderate to severe stroke group was significantly higher than that in the mild stroke group (1.36 ± 0.29 mg/L vs.1.21 ±0.23 mg/L;t =3.902,P ＜ 0.001),the serum cystatin C level in the poor outcome group was significantly higher than that in the good outcome group (1.38 ± 0.25 mg/L vs.1.22 ± 0.25 mg/L;t =4.101,P =0.001).Multivariate logistic regression analysis showed that the serum cystatin C level was an independent risk factor for stroke severity (odds ratio 12.182,95％ confidence interval 11.163-13.202;P ＜ 0.001) and short-term poor outcome (odds ratio 9.025,95 ％ confidence interval 8.202-9.848;P ＜ 0.001).Conclusion The serum cystatin C level is significantly correlated with the severity of stroke and the short-term outcome in patients with acute ischemic stroke.

Objective To investigate the relationship betw een the serum bilirubin level and the severity of disease and short-term outcome in patient w ith acute ischemic stroke. Methods A total of 120 consecutive inpatients w ith acute ischemic stroke w ere enroled and 105 healthy subjects at the same time w ere used as a control group. The biochemical indicators, such as serum total bilirubin, direct bilirubin, indirect bilirubin, blood lipid, and blood glucose w ere measured w ithin 24 h after admission. The National Institutes of Health Stroke Scale ( NIHSS ) w as used to assess the neurological deficits on the day of admission. The NIHSS score <8 w as defined as mild stroke and ≥8 w as defined as moderate to severe stroke. At discharge or 14 d after onset, the modified Rankin Scale (mRS) w as used to evaluate the clinical outcomes, 0-2 w as defined as good outcome and > 2 w as defined as poor outcome. The levels of serum total bilirubin, direct bilirubin, and indirect bilirubin w ere measured again. Results The levels of serum total bilirubin, direct bilirubin, and indirect bilirubin in the moderate to severe stroke group w ere significantly higher than those in the mild stroke group ( P <0.01) and the control group ( P <0.01). Multivariate logistic regression analysis show ed that the increased levels of serum total bilirubin (odds ratio [OR] 1.855,95%confidence interval [CI] 1.390-2.475; P <0.01), indirect bilirubin ( OR 3.380, 95%CI 1.271-11.901; P <0.05), and direct bilirubin ( OR 3.51, 95%CI 1.062-11.473; P <0.01) had significantly independent correlation w ith baseline disease severity. Univariate analysis show ed that the increased serum total bilirubin level on admission w as associated w ith the short-term poor outcome ( P <0.05), but after adjustment for other confounding factors, there w as no statistical significance ( OR 2.411, 95%CI 0.803-7.243, P >0.05). Conclusions The serum bilirubin level show ed stress increase in patients w ith cerebral infarction in acute phase; and it w as significantly associated w ith the degree of neurological deficit, but it w as not associated w ith short-term outcome. It might be a defense response to the body for stroke events.

OBJECTIVETo investigate the effect of quercetin on apoptosis and feedback regulation of MDM2-p53 in multiform glioblastoma U87 cells in vitro.

METHODSU87 cells exposed to different concentrations of quercetin (50, 100, and 150 µmol/L) were examined with flow cytometry, RT-PCR and Western blotting for detecting the cell apoptosis, MDM2 mRNA expression, and p53 and caspase-3 expressions.

RESULTSQuercetin induced obvious apoptosis in U87 cells in a concentration-dependent manner, with apoptosis rates of (12.40∓0.70)% at Q0, (22.53∓0.72)% at Q50, (29.06∓0.81)% at Q100, and (31.5∓0.45)% at Q150. Quercetin significantly increased the expressions of MDM2 mRNA and active caspase-3 protein but decreased the expression of p53 in the cells.

CONCLUSIONQuercetin promotes the apoptosis of multiform glioblastoma U87 cells mediated by caspase-3 and influences the feedback balance of MDM2-p53.

Apoptosis ; Caspase 3 ; metabolism ; Cell Line, Tumor ; drug effects ; Glioma ; metabolism ; pathology ; Humans ; Proto-Oncogene Proteins c-mdm2 ; metabolism ; Quercetin ; pharmacology ; Tumor Suppressor Protein p53 ; metabolism

OBJECTIVETo investigate the influence of exposure to different concentrations of ethanol on neural progenitor cells and the differentiation of neurons and glial cells in zebrafish embryos.

METHODSZebrafish embryos were exposed to 1%, 2%, and 2.5% (V/V) ethanol at 5 hpf by adding ethanol to the egg water. In situ hybridization and real-time PCR were used to detect the changes in the mRNA expression profiles of the markers of different cells to examine the effects of alcohol on neural development.

RESULTSThe number of neural precursor cells, neurons and mature glial cells was significantly reduced in the zebrafish embryos following ethanol exposure, and this reduction became more prominent as the ethanol concentration increased. The expression of the early glial marker slc1a3a was down-regulated in the spinal cord but increased in the brain after exposure to increased ethanol concentrations. The expression of the mature glial markers was significantly lowered in response to exposure to increasing ethanol concentrations.

CONCLUSIONSEthanol can reduce neural precursor cells and inhibits neuronal and glial differentiation in zebrafish embryos.

Animals ; Brain ; Cell Differentiation ; drug effects ; Embryo, Nonmammalian ; drug effects ; Ethanol ; adverse effects ; Neural Stem Cells ; drug effects ; Neurogenesis ; drug effects ; Neuroglia ; drug effects ; Neurons ; drug effects ; Spinal Cord ; Zebrafish ; embryology

Objective To investigate the effect of quercetin on apoptosis and feedback regulation of MDM2-p53 in multiform glioblastoma U87 cells in vitro. Methods U87 cells exposed to different concentrations of quercetin (50, 100, and 150μmol/L) were examined with flow cytometry, RT-PCR and Western blotting for detecting the cell apoptosis, MDM2 mRNA expression, and p53 and caspase-3 expressions. Results Quercetin induced obvious apoptosis in U87 cells in a concentration-dependent manner, with apoptosis rates of (12.40 ± 0.70)% at Q0, (22.53 ± 0.72)% at Q50, (29.06 ± 0.81)% at Q10 , and (31.5 ± 0.45)% at Q150. Quercetin significantly increased the expressions of MDM2 mRNA and active caspase-3 protein but decreased the expression of p53 in the cells. Conclusion Quercetin promotes the apoptosis of multiform glioblastoma U87 cells mediated by caspase-3 and influences the feedback balance of MDM2-p53.

Objective To investigate the influence of exposure to different concentrations of ethanol on neural progenitor cells and the differentiation of neurons and glial cells in zebrafish embryos. Methods Zebrafish embryos were exposed to 1%, 2%, and 2.5%(V/V) ethanol at 5 hpf by adding ethanol to the egg water. In situ hybridization and real-time PCR were used to detect the changes in the mRNA expression profiles of the markers of different cells to examine the effects of alcohol on neural development. Results The number of neural precursor cells, neurons and mature glial cells was significantly reduced in the zebrafish embryos following ethanol exposure, and this reduction became more prominent as the ethanol concentration increased. The expression of the early glial marker slc1a3a was down-regulated in the spinal cord but increased in the brain after exposure to increased ethanol concentrations. The expression of the mature glial markers was significantly lowered in response to exposure to increasing ethanol concentrations. Conclusion Ethanol can reduce neural precursor cells and inhibits neuronal and glial differentiation in zebrafish embryos.

Objective To investigate the effect of quercetin on apoptosis and feedback regulation of MDM2-p53 in multiform glioblastoma U87 cells in vitro. Methods U87 cells exposed to different concentrations of quercetin (50, 100, and 150μmol/L) were examined with flow cytometry, RT-PCR and Western blotting for detecting the cell apoptosis, MDM2 mRNA expression, and p53 and caspase-3 expressions. Results Quercetin induced obvious apoptosis in U87 cells in a concentration-dependent manner, with apoptosis rates of (12.40 ± 0.70)% at Q0, (22.53 ± 0.72)% at Q50, (29.06 ± 0.81)% at Q10 , and (31.5 ± 0.45)% at Q150. Quercetin significantly increased the expressions of MDM2 mRNA and active caspase-3 protein but decreased the expression of p53 in the cells. Conclusion Quercetin promotes the apoptosis of multiform glioblastoma U87 cells mediated by caspase-3 and influences the feedback balance of MDM2-p53.

Objective To investigate the influence of exposure to different concentrations of ethanol on neural progenitor cells and the differentiation of neurons and glial cells in zebrafish embryos. Methods Zebrafish embryos were exposed to 1%, 2%, and 2.5%(V/V) ethanol at 5 hpf by adding ethanol to the egg water. In situ hybridization and real-time PCR were used to detect the changes in the mRNA expression profiles of the markers of different cells to examine the effects of alcohol on neural development. Results The number of neural precursor cells, neurons and mature glial cells was significantly reduced in the zebrafish embryos following ethanol exposure, and this reduction became more prominent as the ethanol concentration increased. The expression of the early glial marker slc1a3a was down-regulated in the spinal cord but increased in the brain after exposure to increased ethanol concentrations. The expression of the mature glial markers was significantly lowered in response to exposure to increasing ethanol concentrations. Conclusion Ethanol can reduce neural precursor cells and inhibits neuronal and glial differentiation in zebrafish embryos.

OBJECTIVETo explore the effect of quercetin on the invasion, migration, proliferation and cell cycle of glioma U87 cells.

METHODSGlioma U87 cells were treated with 50, 100, or 150 µmol/L quercetin (Q(50), Q(100) and Q(150) groups, respectively) or with DMSO (Q(0) group). Transwell in vitro invasion and migration assays, Click-iT Edu test and flow cytometry were performed to evaluate the effect of quercetin on the invasion, migration, proliferation and cell cycle of U87 cells.

RESULTSAfter 36 h of quercetin treatment, the cells in Q(50), Q(100) and Q(150) groups showed invasive cell percentages (relative to Q(0) group) of 52.08%, 24.63%, and 13.13%, respectively (P<0.05). After quercetin treatment for 12 h, the migrating cell percentages (relative to Q(0) group) in Q(50), Q(100) and Q(150) groups were 49.46%, 26.78%, and 14.56%, respectively (P<0.05). After 24 h of quercetin treatment, the cell proliferation ratios in Q(0), Q(50), Q(100) and Q(150) groups were 25.21%, 18.38%, 16.74% and 15.24%; the cell percentages in phase G0/Gl were 71.14%, 72.71%, 69.29%, and 66.47%, phase S were 25.32%, 22.48%, 21.96%, and 23.32%, and phase G(2)/M were 3.53%, 4.80%, 8.75%, and 10.25% in the 4 groups, respectively, showing a significant difference between groups Q(100), Q(150) and group Q(0) in phase G(2)/M cell percentages (P<0.05).

CONCLUSIONSQuercetin can significantly inhibit the invasion, migration and proliferation of glioma U87 cells by blocking the cell cycle progression.

Cell Cycle ; drug effects ; Cell Line, Tumor ; Cell Movement ; drug effects ; Cell Proliferation ; drug effects ; Glioma ; pathology ; Humans ; Quercetin ; pharmacology