Reactive oxygen species (ROS) play a very important role in vascular homeostasis both physiologically and pathophysiologically. The imbalance between production and metabolism of ROS contributes to various vascular diseases. Recent studies have demonstrated that ROS regulated the redox-sensitive protein kinases in the signal transduction pathways,affected the activities of these kinases, and thus modulated the gene expression.

AIM To study the protective effect of total salvianolic acid against cerebral ischemia reperfusion injury. METHODS The cerebral ischemia reperfusion model in mice was made by means of ligating bilateral common carotid arteries in mice. After reperfusion, latency, error number of step down test and the gasping time after cutting head in ischemia reperfusion mice were recorded. Spectrophotometric assay were used to measure the activity of superoxide dismutase (SOD), the contents of malondialdehyde (MDA) and glutathione peroxidase (GSH) in brain of experimental mice brain homogenate. RESULTS In step down test, the ischemia reperfusion impaired the function of learning and memory in mice. The total salvianolic acid markedly improved the function of learning and memory, reduced the error number and extended the latency in ischemia reperfusion mice. The total salvianolic acid also significantly inhibited the changes of SOD, MDA and GSH in the cerebrum induced by ischemia reperfusion. CONCLUSION The total salvianolic acid has protective effects against cerebral ischemia reperfusion injury via its antioxidant activity.

AIM To study the protective effect of total salvianolic acid against cerebral ischemia reperfusion injury. METHODS The cerebral ischemia reperfusion model in mice was made by means of ligating bilateral common carotid arteries in mice. After reperfusion, latency, error number of step down test and the gasping time after cutting head in ischemia reperfusion mice were recorded. Spectrophotometric assay were used to measure the activity of superoxide dismutase (SOD), the contents malondialdehyde (MDA) and glutathione peroxidase (GSH) in brain of experimental mice brain homogenate. RESULTS In step down test, the ischemia reperfusion impaired the function of learning and memory in mice. The total salvianolic acid markedly improved the function of learning and memory, reduced the error number and extended the latency in ischemia reperfusion mice. The total salvianolic acid also significantly inhibited the changes of SOD, MDA and GSH in the cerebrum induced by ischemia reperfusion. CONCLUSION The total salvianolic acid has protective effect against cerebral ischemia reperfusion injury via its antioxidant activity.

OBJECTIVETo investigate the effect of polysaccharide sulfate 916 (PS916) on the production of nitric oxide (NO) in ECV304 cells induced by tumor necrosis factor-alpha (TNF alpha), interleukin-1 beta (IL-1 beta) and H(2)O(2) in vitro.

METHODSProduction of NO in ECV304 cells was measured by the Griess method and the proliferation of cells was tested by the MTT method. The activity of NO synthase was detected spectrophotometrically.

RESULTSProduction of NO in ECV304 cells decreased after treatment with 40 ng/ml IL-1 beta and 40 ng/ml TNF alpha, but increased in the presence of H(2)O(2) 0.1 mmol/L. PS916 significantly enhanced NO production in ECV304 cells in a dose-dependent manner in the TNF alpha and IL-1 beta treated groups and decreased it in the H(2)O(2) treated group. Proliferation of ECV304 cells was inhibited by TNFalpha and H(2)O(2) and no effect was found in the IL-1 beta treated group. PS916 increased the proliferation of cells treated with TNFalpha and H(2)O(2) dose-dependently. In vitro, PS916 has no effect on the activity of NO synthase.

CONCLUSIONPS916 has a protective effect on ECV304 cells exposed to IL-1 beta, TNF alpha and H(2)O(2).

Cell Division ; drug effects ; Cell Line ; Cytokines ; pharmacology ; Dose-Response Relationship, Drug ; Endothelium, Vascular ; cytology ; drug effects ; metabolism ; Humans ; Hydrogen Peroxide ; pharmacology ; Interleukin-1 ; pharmacology ; Nitric Oxide ; biosynthesis ; Nitric Oxide Synthase ; drug effects ; metabolism ; Polysaccharides ; metabolism ; pharmacology ; Sulfuric Acids ; metabolism ; Tumor Necrosis Factor-alpha ; pharmacology

OBJECTIVETo investigate the effects of salvianolic acids on human umbilical vein endothelial cells (HUVEC) against damage induced by cholestane-3beta-5alpha-6beta-triol (chol-triol).

METHODSThe viability of HUVEC was measured by MTT method. The apoptosis of HUVEC induced by chol-triol was detected by flow cytometry and TUNEL assay. The production of malondialdehyd (MDA) in HUVEC was tested by thiobarbaturic acid (TBA) assay.

RESULTSThe viability of HUVEC treated with chol-triol 100 micro mol/L decreased by 39.8% while salvianolic acids 100 micro g/ml increased by 27.9%. The apoptotic rate of HUVEC measured by PI staining increased from 6% - 8% to 17% - 20% after chol-triol treatment for 12 h. Salvianolic acids 100 micro g/ml reduced the apoptotic rate to 10% - 14% after treatment HUVEC for 1 h prior to chol-triol treatment. In another experiment, chol-triol increased the number of TUNEL-positive cells 5 times, but salvianolic acids 10 micro g/ml and 100 micro g/ml reduced the number of TUNEL-positive cells by 36.9% and 61.2%, respectively. The production of MDA in HUVEC increased by 120.7% after chol-triol treatment for 12 h. Salvianolic acids 10 micro g/ml and 100 micro g/ml also decreased the concentration of MDA by 28.7% and 39.8%, respectively.

CONCLUSIONSalvianolic acids has protective effect on endothelial cells against damage induced by chol-triol.

Apoptosis ; drug effects ; Benzofurans ; pharmacology ; Caffeic Acids ; pharmacology ; Cell Survival ; drug effects ; Cells, Cultured ; Cholestanols ; toxicity ; Cinnamates ; pharmacology ; Depsides ; Endothelium, Vascular ; cytology ; drug effects ; Humans ; Lactates ; pharmacology ; Malondialdehyde ; metabolism

OBJECTIVETo study the effect of polysaccharide sulfate 916 (PS916) on neutrophil-endothelial cell adhesion.

METHODSCell adhesion was evaluated by testing neutrophil myeloperoxidase activity. Expression of adhesion molecule in human umbilical vein endothelial cell (HUVEC) was measured by ELISA. The neutrophil activation rate induced by N-formyl-methionyl-leucyl-phenylalanine (fMLP) was tested by nitroblue tetrazolium (NBT) reduction.

RESULTSTumor necrosis factor alpha (TNFalpha, 50 - 800 U/ml) increased the adherence of neutrophil to TNFalpha-stimulated HUVEC in a concentration and time dependent manner. PS916 (0.01 - 1.0 mg/ml) dose-dependently inhibited the adherence of neutrophils to TNFalpha-stimulated HUVEC. fMLP increased the activation rate of neutrophils independent of concentration. PS916 also inhibited the adherence of fMLP-activated neutrophils to HUVEC. Moreover, PS916 inhibited adhesion molecule expression in TNFalpha-stimulated HUVEC.

CONCLUSIONSPS916 inhibited neutrophil-endothelial adhesion. The mechanism of its action was partially related to suppressing the expressions of intercellular adhesion molecule-1 (ICAM-1) and vascular adhesion molecule-1 (VCAM-1).

Animals ; Cell Adhesion ; drug effects ; Cells, Cultured ; Endothelium, Vascular ; cytology ; Humans ; Intercellular Adhesion Molecule-1 ; analysis ; N-Formylmethionine Leucyl-Phenylalanine ; pharmacology ; Neutrophils ; drug effects ; physiology ; Polysaccharides ; pharmacology ; Rats ; Rats, Wistar ; Sulfuric Acids ; pharmacology ; Tumor Necrosis Factor-alpha ; pharmacology ; Vascular Cell Adhesion Molecule-1 ; analysis