OBJECTIVETo study the effect of Xiaoyu Tablet (XYT) on blood flow parameters and morphology of carotid artery in atherosclerotic patients.

METHODSUsing color Doppler ultrasonographic technique to examine the blood flow parameters and intimal thickness of carotid artery in 20 patients of carotid atherosclerosis after 24 weeks treatment of XYT, and compared with those in 10 patients treated with gastrodine lipid-lowering tablet.

RESULTSAfter 24 weeks treatment, blood flow parameters of carotid artery were obviously improved and intimal thickness of common carotid arteries in both side was markedly decreased. XYT showed an effect better than that of gastrodine lipid-lowering tablet.

CONCLUSIONXYT is effective in increasing blood flow of cervical and cerebral arteries.

Arteriosclerosis ; diagnostic imaging ; drug therapy ; physiopathology ; Blood Flow Velocity ; Carotid Arteries ; diagnostic imaging ; pathology ; Carotid Stenosis ; diagnostic imaging ; pathology ; Drugs, Chinese Herbal ; therapeutic use ; Female ; Humans ; Male ; Middle Aged ; Phytotherapy ; Tablets ; Tunica Intima ; pathology ; Ultrasonography, Doppler, Color

Animals ; Arteriosclerosis ; drug therapy ; Cholesterol, LDL ; blood ; Drugs, Chinese Herbal ; pharmacology ; Hyperlipidemias ; drug therapy ; Lipids ; blood ; Lipoproteins ; blood ; Lipoproteins, LDL ; blood ; Male ; Rabbits ; Tablets ; Triglycerides ; blood

AIMTo study the effects of ferulic acid (FA) on E-selectin expression in human umbilical vein endothelial cells (HUVECs) activated by lipopolysaccharide and leukocyte-endothelial cell adhesion.

METHODSThe effects of FA on E-selectin and E-selectin mRNA expression were determined by flow cytometry and reverse transcription polymerase chain reaction. The effect of FA on HL60-HUVEC adhesion was evaluated with the method of staining the cells by Rose Bengal.

RESULTSThe expression of E-selectin and E-selectin mRNA were down regulated by FA (0.62 and 0.41 mmol x L(-1), respectively). HL60 cells adhered to activated HUVECs were also reduced by FA (0.62 and 0.41 mmol x L(-1), respectively).

CONCLUSIONFA can inhibit the expression of E-selectin and E-selectin mRNA and HL60-HUVEC adhesion. This may contribute to its protective effect against ischemia-reperfusion injury.

Cell Adhesion ; drug effects ; Cells, Cultured ; Coumaric Acids ; pharmacology ; E-Selectin ; biosynthesis ; genetics ; Endothelial Cells ; metabolism ; HL-60 Cells ; physiology ; Humans ; RNA, Messenger ; biosynthesis ; genetics ; Umbilical Veins ; cytology

AIMTo observe the effect of quercetin (Que) on the adhesion of platelets to cultured endothelial cells and adhesion molecule expression by human umbilical vein endothelial cells (HUVEC) and platelets.

METHODS[3H]-Adenine labeled platelets were incubated with HUVEC to investigate the effect of Que on adhesion of platelets to HUVEC. The number of platelets adhering to the HUVEC monolayer was determined by liquid scintillation spectroscopy. TNF-alpha induced HUVEC expression ICAM-1 and thrombin induced platelets expression of P-selectin were measured by flow cytometry.

RESULTSQue (0.3-2.4 mumol.L-1) was shown to inhibit the increase of P-selectin expression of thrombin activated platelets. Pretreatment of HUVEC with tumor necrosis factor (TNF-alpha) significantly increased platelets adhesion to HUVEC and the expression ICAM-1. Que (0.6-2.4 mumol.L-1) inhibited this effect of TNF-alpha in a concentration-dependent manner.

CONCLUSIONQue can inhibit the adhesion of platelets to HUVEC and the expression of adhesion molecules (P-selectin and ICAM-1).

Blood Platelets ; drug effects ; metabolism ; Cell Adhesion ; drug effects ; Cells, Cultured ; Endothelium, Vascular ; drug effects ; metabolism ; Gene Expression ; drug effects ; Humans ; Intercellular Adhesion Molecule-1 ; metabolism ; P-Selectin ; metabolism ; Quercetin ; pharmacology ; Umbilical Veins ; cytology

The recent progress in neural stem cells (NSCs) research has shed lights on possibility of repair and restoration of neuronal function in neurodegenerative diseases using stem cells. Induction of stem cells differentiate into mature neurons is critical to achieve the clinical applications of NSCs. At present, molecular mechanisms modulating NSC differentiation are not fully understood. Differentiation of stem cells into neuronal and glial cells involves an array of changes in expression of transcription factors. Transcription factors then trigger the expression of a variety of central nervous system (CNS) genes that lead NSCs to differentiate towards different cell types. In this paper, we summarized the recent findings on the gene regulation of NSCs differentiation into neuronal cells.

OBJECTIVETo investigate the effects of adenovirus-mediated PTEN and P27 on the invasion of PC-3 in vitro and angiogenesis, along with their synergy in the treatment of prostate cancer.

METHODSRecombinant adenovirus vectors of the human tumor suppressor genes PTEN and P27 were constructed. The replication-incompetent recombinant adenovirus was packaged and propagated in HEK293 cells. The viral titer was examined by plaque assay and the mRNA and protein expressions of PTEN and P27 in human prostate cancer cell line PC-3 infected with Ad-PTEN and Ad-P27 were determined by RT-PCR and Western blot respectively. The invasion of PC-3 cells in vitro was examined by Boyden chamber assay. MTT assay was used to testify the effect of supernatant from PC-3 infected with Ad-PTEN and Ad-P27 on the proliferation of endothelial cells ECV-304 and the CAM test was used to testify the effect of PTEN and P27 on angiogenesis. The difference between the combined therapy group and the single gene therapy group was also examined.

RESULTSThe viral titers of Ad-PTEN and Ad-P27 were 1.8 x 10(7) pfu/ml and 1.2 x 10(9) pfu/ml respectively. Adenovirus infection verified that the mRNA and protein expression of PTEN and P27 were steady in human PC-3 cells. The invasion in vitro of PC-3 cells was significantly inhibited by infection with Ad-PTEN or/and Ad-P27. CAM and MTT assays of ECV-304 confirmed that the supernatant from PC-3 cells infected with Ad-PTEN or/and Ad-P27 could inhibit the angiogenesis effectively. There was a significant difference between the combined therapy group and the single gene therapy group.

CONCLUSIONThe combined gene therapy of Ad-PTEN and Ad-P27 plays a synergistic role in inhibiting the invasiveness of PC-3 cells and angiogenesis.

Adenoviridae ; genetics ; Cell Line, Tumor ; Cyclin-Dependent Kinase Inhibitor p27 ; genetics ; Humans ; Male ; Neoplasm Invasiveness ; PTEN Phosphohydrolase ; genetics ; Prostatic Neoplasms ; blood supply ; pathology ; Transfection

Ketamine is a phencyclidine derivative acting primarily as a noncompetitive antagonist of N-methyl-D-aspartate (NMDA) excitatory glutamate receptors. As a common intravenous anaesthetic in clinic, it is also increasingly abused because of its hallucination and addiction effects. Based on the pharmacological and toxicologic characteristics of ketamine and the acknowledged addiction mechanism of other abused drugs, this article reviews the possible addiction mechanism of the ketamine in the aspects of its enhanced effects and reward systems, the anatomic structures, the related receptors and the individual differences.
Anesthetics, Dissociative/adverse effects* ; Animals ; Brain/drug effects* ; Humans ; Illicit Drugs ; Ketamine/adverse effects* ; Mental Disorders/chemically induced* ; Rats ; Receptors, Dopamine/drug effects* ; Receptors, N-Methyl-D-Aspartate/drug effects* ; Substance-Related Disorders

Schizophrenia is one of the common mental diseases. Because the mechanism of the schizophrenia is significantly complicated, the cause is still unknown. N-methyl-D-aspartate receptor antagonist can simulate the positive and negative symptoms, as well as the cognitive disorder of schizophrenia. Thus it has been widely used to establish the animal models of schizophrenia. The relationship of the three blocking agents of ion channels (phencyclidine, MK-801, ketamine) and the establishment of schizophrenia animal models is reviewed in this article.
Animals ; Behavior, Animal/drug effects* ; Brain/physiopathology* ; Consciousness Disorders/physiopathology* ; Disease Models, Animal ; Dizocilpine Maleate/pharmacology* ; Excitatory Amino Acid Antagonists/pharmacology* ; Humans ; Ketamine/pharmacology* ; Mice ; Phencyclidine/pharmacology* ; Rats ; Receptors, N-Methyl-D-Aspartate/antagonists & inhibitors* ; Schizophrenia/physiopathology*

BACKGROUNDThe effects of triterpenic acid from Prunella vulgaris L. (TAP) on diabetes and its mechanism are uncertain. The aim of this study was to investigate the effects of TAP on antihyperglycemic, antioxidant, and pancreas-protective in streptozotozin (STZ)-diabetic rats.

METHODSThe diabetic model was produced by injection of 60 mg/kg STZ. Blood was drawn from the tail vein of rats after 72 hours. Rats with blood glucose ≥ 16.7 mmol/L were considered diabetic. Diabetic rats were randomly divided into four groups: (1) Diabetes rat (STZ), (2) Diabetic rats treated with 50 mg/kg of triterpenic acid from Prunella vulgaris L (STZ + TAP50), (3) Diabetic rats treated with 100 mg/kg TAP (STZ + TAP100), and (4) Diabetic rats treated with 200 mg/kg TAP (STZ + TAP200). Normal rats (n = 10) acted as the control group (NC). TAP was administered by the intragastric route once each day for six weeks. Body weight and the concentration of blood glucose (BG) were measured after three and six weeks. Fructosamine (FMN), malondialdehyde (MDA), and nitric oxide (NO), and the activities of nitric oxide synthase (NOS) and superoxide dismutase (SOD) in serum were determined after six weeks using commercially available kits following the manufacturer's instructions. Pathologic changes in pancreatic β-cells were also investigated by microscopic examination after hematoxylin-eosin (HE) staining. The level of SOD mRNA in pancreatic β-cells was measured by polymerase chain reaction (PCR).

RESULTSThe levels of BG, FMN, NO, and MDA and the activities of NOS in serum in the four diabetes groups were significantly increased compared with the control group (P < 0.01). The activity of SOD in serum and the body weight was significantly decreased compared with the control group (P < 0.01). After administration of TAP to diabetic rats for six weeks, the body weight and the levels of BG, FMN, MDA, NO and the activity of NOS in serum decreased significantly compared with the STZ group in a dose-dependent manner. The activity of SOD in serum and body weight increased significantly compared with the STZ group in a dose-dependent manner. In addition, diabetic rats showed a significant decrease in SOD mRNA expression in pancreatic β cells. However, these changes were reversed by TAP. Histopathological examination also showed the protective effect of TAP on pancreatic β cells.

CONCLUSIONSTriterpenic acid from Prunella vulgaris L. has an anti-diabetic effect, by controlling blood glucose and antioxidants, and has a protective effect on the pancreas.

Animals ; Blood Glucose ; analysis ; Diabetes Mellitus, Experimental ; drug therapy ; metabolism ; Insulin-Secreting Cells ; drug effects ; pathology ; Male ; Prunella ; chemistry ; RNA, Messenger ; analysis ; Rats ; Rats, Sprague-Dawley ; Streptozocin ; Superoxide Dismutase ; genetics ; Triterpenes ; therapeutic use

OBJECTIVETo establish a BCR/ABL+ cell line with resistance to imatinib, and investigate the possible mechanisms of the acquired resistance.

METHODSK562 cells were cultured in gradually increased concentrations of imatinib over a period of several months to generate their resistance line. MTT assay, RT-PCR, Western blotting, and FISH were used to study the possible molecular mechanisms of the resistance.

RESULTSA resistant cell line, K562/G01, was established with 15.2 +/- 3.0-fold resistant to imatinib as compared with that of the parental sensitive cell line. The resistant cell line also had the cross-resistance to a broad spectrum of other anticancer agents excepting for DOX. There was no difference between the two cell lines in terms of the cell morphology, proliferation doubling time, and fraction distribution of cell cycle. K562/G01 cells showed increased levels of BCR/ABL, mdr1 mRNA and their coding proteins and the increased tyrosine kinase activity. No point mutation in the BCR/ABL ATP-binding site was detected while the copies of BCR/ABL fusion gene were increased in K562/G01 cells.

CONCLUSIONAn imatinib-resistant human leukemia cell line, K562/G01, was established. The mechanisms of resistance of K562/G01 cells to imatinib involved increased expression of BCR/ABL and mdr1/P-gp, amplification of BCR/ABL fusion gene, and increased activity of BCR/ABL.

ATP-Binding Cassette, Sub-Family B, Member 1 ; genetics ; metabolism ; Antineoplastic Agents ; pharmacology ; Benzamides ; Drug Resistance, Neoplasm ; Drug Screening Assays, Antitumor ; Fusion Proteins, bcr-abl ; genetics ; metabolism ; Humans ; Imatinib Mesylate ; K562 Cells ; drug effects ; metabolism ; Piperazines ; pharmacology ; Pyrimidines ; pharmacology