Aim The effect and mechanism of human placental extract(HPE) on the lipoprotein-cholesterol metabolism, peroxidation and the function of platelet aggregation in hyperlipaemia rats were abserved.Methods Wistar rat with hyperlipaemia models were given each HPE 0.4 ml (100 g)-1?d-1 through lavage for 12 days.The serum levels of TG,TC,LDL-C,HDL-C and HDL2-C in its subgroup were measured.The activies of LPO and SOD in both blood and liver tissue were determined .The effect of HPE on lipidosis of liver were abserved by fat dyeing.The levels of 6-keto-PGF1?,TXB2 in plasma and maximum platelet aggregation rate were measured by ELASA. Result The levels of HDL-C and HDL2-C were increased (P

Emergencies ; Environmental Exposure ; standards ; Humans ; Maximum Allowable Concentration

Humans ; Laryngoscopy ; Larynx ; Magnetic Resonance Imaging ; Tomography Scanners, X-Ray Computed ; Tuberculosis, Laryngeal ; diagnosis

OBJECTIVETo investigate the therapeutic mechanism of three-step sequential method (TSSM) on patients with corticosteroid-dependent asthma (SDA).

METHODSForty patients with SDA were randomly assigned according to the randomizing number table to two groups equally, the treated group treated with three-step sequential recipes plus inhalation of Pulmicort Turbuhaler 200 microg, twice a day, and the control group treated with Pulmicort Turbuhaler alone. The therapeutic course for both groups was 12 - 14 weeks. Changes of the symptom score of asthma, the corticosteroid dosage used and the lung function were observed and the positive expression rate of IFN-gamma and IL-4 in peripheral CD4+ T cells were determined by flow cytometry before and after treatment.

RESULTSThere was significant difference in the asthma symptom score, the oral corticosteroid dosage and the lung function between the treated group and the control group after treatment (P < 0.01). The expression rate of Th2 reduced, the ratio of Th1/Th2 increased significantly after treatment in both groups (P < 0.01, P < 0.05), but the changes were more remarkable in the treated group than those in the control group, showing significant difference between them (P < 0.01), while the expression rate of Th1 had no obvious change after treatment with no significant difference shown between the two groups (P > 0.05).

CONCLUSIONTSSM can regulate imbalance of Th1/Th2, inhibit generation of inflammatory cytokines, decrease airway hyper-response, and therefore improve the pulmonary function, alleviate the asthmatic symptoms and reduce the patients' dependence on corticosteroid.

Adult ; Asthma ; drug therapy ; Drugs, Chinese Herbal ; administration & dosage ; therapeutic use ; Female ; Glucocorticoids ; adverse effects ; therapeutic use ; Humans ; Male ; Middle Aged ; Phytotherapy ; methods ; Substance-Related Disorders ; drug therapy ; etiology ; T-Lymphocyte Subsets ; drug effects ; T-Lymphocytes, Helper-Inducer ; drug effects

Objective To explore hemodynamic parameter changes in pulmonary arterial hypertension(PAH)treated by transplantation of bone marrow mesenchymal stem cells(MMSCs)in the experimental rats.Methods MMSCs cells were collected from bone marrow of Sprague-Dawleye(SD)rat's femoral and tibial bones,cultured and passaged in vitro,then stained by Hoechst 33342 fluorescence dye stuff.Ninety healthy male SD rats were randomly divided into 3 groups(n=30):normal control group(group N),MMSCs transplanted group(group M),PAH model group(group H).The rats in the two latter groups were given a single subcutaneous crotaline(50 mg/kg)to establish the model of PAH.The rats of group N were injected respectively a single subcutaneous 9 g/L saline water(6 mL/kg).After 21 days,5?109 L-1 MMSCs cultured in 1 mL phosphate-buffered saline were infused into the rats respectively in group M by sublingual vein and 1 mL L-DMEM was given in group H.The indexalso of right ventricle systolic pressure(RVSP),right ventricle hypertrophy index,arterial blood gas analysis and the changes of small pulmonary blood vessel were observed after 28 days.Results The administration of MMSCs 28 days after PAH nearly completely prevented the increase in RVSP with PAH alone [(32.20?2.32)mmHg vs(48.30?1.56)mmHg P

0.05).Conclusions SNP of 2350G→A in ACE gene is associated with MI,AA genotype is probably a genetic marker of MI in Han nationality.

OBJECTIVETo investigate the changes of vasoconstriction and vasodilatation under different temperature conditions and the protective effects of Vitamin E (Vit E) against endothelial injury induced by hypothermia.

METHODSThe tail arterial rings were prepared for isometric tension recording using multi wire myograph system. The effect of temperature on relaxation and construction was evaluated. Incubate the arterial rings with different concentration of Vit E when they were exposed to hypothermia, then acetylcholine (ACh)-induced endothelium-dependent relaxation was investigated to evaluate the activity of endothelial.

RESULTS(1) The hypothermia could enhanced the dose-dependent construction induced by PE in mice tail artery. (2) Exposure to hypothermia also resulted in increase of sodium nitroprusside (SNP)-induced re-After incubation with Vit E, the vascular relaxation responses to ACh increased in an endothelium-dependent manner, when compared with the hypothermia-treated group.

CONCLUSIONThe vascular function of constriction was attenuated by hypothermia, while the relaxation was increased. Vit E could prevent the hypothermia-induced decrease in vascular endothelial cells.

Animals ; Arteries ; drug effects ; physiology ; Cold Temperature ; Hypothermia ; In Vitro Techniques ; Male ; Mice ; Prazosin ; pharmacology ; Solanaceous Alkaloids ; pharmacology ; Vasoconstriction ; drug effects ; Vasodilation ; drug effects ; Vasodilator Agents ; pharmacology ; Vitamin E ; pharmacology

This study is to investigate the protection effect of schisandrin B (Sch B) against oxidation stress of HK-2 cells induced by cisplatin and the mechanisms involved. HK-2 cells were cultured and divided into different groups: solvent control group, cisplatin exposure group, positive group, Sch B treatment group. Cell viability and toxicity were evaluated by MTT and LDH assay. GSH level and SOD enzymes activities were also measured. DCFH-DA as fluorescence probe was used to detect ROS level by fluorescence microplate reader. Nrf2 translocation was detected by Western blotting. Real time Q-PCR was used to detect expressions of NQO1, HO-1 and GCLC mRNA level. The results showed that Sch B could significantly inhibit the decline of cell viability induced by cisplatin treatment (P < 0.05) and the protective effect was in a dose dependent manner. Furthermore, Sch B treatment significantly inhibited the increase of ROS level induced by cisplatin and reversed the decrease of GSH level (P < 0.05). When Sch B concentration was up to 5 micromol x L(-1), SOD enzyme activities were also enhanced significantly compared with that of the cisplatin group (P < 0.05). It was shown that Sch B could cause nuclear accumulation of Nrf2 in association with downstream activation of Nrf2 mediated oxidative response genes such as GCLC, NQO1 and HO-1. These results suggested Sch B could protect against the oxidative damage of HK-2 cells induced by cisplatin via the activation of Nrf2/ARE signal pathway.
Antineoplastic Agents ; toxicity ; Antioxidants ; isolation & purification ; pharmacology ; Cell Line ; Cell Survival ; drug effects ; Cisplatin ; toxicity ; Cyclooctanes ; isolation & purification ; pharmacology ; Glutamate-Cysteine Ligase ; genetics ; metabolism ; Glutathione ; metabolism ; Heme Oxygenase-1 ; genetics ; metabolism ; Humans ; Kidney Tubules, Proximal ; cytology ; metabolism ; L-Lactate Dehydrogenase ; metabolism ; Lignans ; isolation & purification ; pharmacology ; NAD(P)H Dehydrogenase (Quinone) ; genetics ; metabolism ; NF-E2-Related Factor 2 ; genetics ; metabolism ; Polycyclic Compounds ; isolation & purification ; pharmacology ; RNA, Messenger ; metabolism ; Reactive Oxygen Species ; metabolism ; Schisandra ; chemistry ; Signal Transduction ; Superoxide Dismutase ; metabolism

OBJECTIVETo investigate the effects of non-neuronal muscarinic receptors (NNMR) stimulation on atherosclerosis and endothelial cells activation.

METHODSAtherosclerosis model was established in ApoE-/- mice by a high fat diet for 7 weeks. During the experimental periods, animals were received a low (7 mg/kg/d) or a high (21 mg/kg/d) dose of arecoline by gavage. At the termination of the treatments, serum total cholesterol and NO levels were measured, and the aorta morphology was analyzed by hematoxylin and eosin staining. The gene expression of monocyte chemoattractant protein-1 (MCP-1) and adhesion molecules in the thoracic aortas was determined by RT-PCR, and the MCP-1 protein expression and NF-κB activity were detected by Western blot analysis. NO production, MCP-1 secretion in cultured rat aortic endothelial cells (RAECs), and monocyte-endothelium adhesion assay were also performed after arecoline treatments.

RESULTSArecoline efficiently decreased atherosclerotic plaque areas, increased serum nitric oxide (NO) content, suppressed the mRNA and protein expression of MCP-1, and modulated the IκB-α degradation and P65 phosphorylation in the aortae of ApoE-/- mice. Furthermore, arecoline promoted NO production and suppressed MCP-1 secretion in cultured RAECs after ox-LDL exposure, and either atropine or NG-nitro-L-arginine methylester could abrogate these effects. Arecoline also significantly inhibited the adherence of U937 monocytes to the ox-LDL injured human umbilical vein endothelial cells, which could be abolished by atropine.

CONCLUSIONOur results indicate that arecoline attenuates the progression of atherosclerosis and inhibits endothelial cells activation and adherence by stimulating endothelial NNMR. These effects, at least in part, are due to its modulation on NF-κB activity.

Animals ; Aorta ; cytology ; Apolipoproteins E ; Arecoline ; pharmacology ; Atherosclerosis ; physiopathology ; prevention & control ; Cell Adhesion Molecules ; metabolism ; Chemokine CCL2 ; metabolism ; Cholesterol ; blood ; Disease Progression ; Endothelial Cells ; cytology ; drug effects ; Endothelium, Vascular ; Human Umbilical Vein Endothelial Cells ; cytology ; Humans ; I-kappa B Proteins ; metabolism ; Lipoproteins, LDL ; Mice ; Mice, Knockout ; Monocytes ; cytology ; NF-KappaB Inhibitor alpha ; Nitric Oxide ; blood ; Nitroarginine ; pharmacology ; Rats ; Receptors, Muscarinic ; physiology ; Transcription Factor RelA ; metabolism

OBJECTIVETo investigate choline promoting angiogenesis on chick embryo chorioallantoic membrane (CAM).

METHODSCAM model was prepared, the choline chloride, human vascular endothelial growth factor (hVEGF) and normal saline were added respectively onto the carrier on the CAM, the state of angiogenesis was observed and the number of new blood vessels was counted.

RESULTSCholine chloride was tested at the concentrations of 0.5 nmol/L - 1 mmol/L in this experiment, when its concentrations were increased to 0.01 micromol/L - 1 000 micromol/L, it could stimulate angiogenesis, the minimum effective concentration was tested as 0.01 micromol/L, and its effect for promoting the angiogenesis was equivalent to that of hVEGF, the potent stimulator for angiogenesis.

CONCLUSIONThe result shows that choline can promote angiogenesis in the chick embryo chorioallantoic membrane.

Animals ; Chick Embryo ; blood supply ; drug effects ; Choline ; pharmacology ; Chorioallantoic Membrane ; blood supply ; drug effects ; Neovascularization, Physiologic ; drug effects