AIM:To explore the effect of β-asarone on vascular endotheliam and adhesion molecule expression of endothelium induced by β-amyloid peptide from Alzheimer's disease and to estimate the injury repair.METHODS:Cultured ECV304 cells were incubated with freshly solublizeal Aβ1-42 and the mixture of Aβ1-42 and β-asarone,the expression of three central adhesion molecules,CD106,CD62P,CE62E and Ca2+ concentration were examined and apoptosis was recorded by Flow eytometry.Test viability of cells by MTT methods.RESULTS:The results showed that in model group and treated group,ligation of endothelial CD106,CD62P,CE62E,markers for endothelial cell activation and Ca2+ concentration,leads to a lot of release.The livability decreased and the apoptosis increased.Further more,simultaneous treatment of ECV304 cells with β-asarone resulted in the decrease significandy in these three adhesion molecules described above and Ca2+ concentration as well as the livability upper and apoptosis lower.CONCLUSION:CD106,CD62P,CE62E,important inflammational factor of Aβ-induced endothelial injury,may be promotion of the inflammatory scade in vascular endothelial.β-asarone may protect ECV304 cell apoptosis by regulate Ca2+ and expression of cell surface markers.

0.05) in the two periods,the ratio of tracheostomy was significantly higher (P

Objective To investigate the effects of ?-asarone,the major constituent of Acorus tarinowii schott,on the expression of endothelial cell adhesion molecules induced by hypoxia and reoxygenation.Methods The expression rates of endothelial cell surface adhesion molecules VCAM-1 and CD62E were detected by flow cytometry(FCM) and specific labeled monoclonal antibody.Results Compared to the normal group,the expression rates of VCAM-1 and CD62E were increased significantly in the model group(hypoxia-reoxygenation group)(P

Objective To observe the effect of ?-asarone combined with eugenol against PC12 cell injury induced by amyloid beta protein (A?25-35) and to explore the advantage of compatibility of monomers in herbs.Methods PC12 cells injury were induced by A?25-35.The morphological features and survival rate of PC12 cells as well as the changes of intracellular Ca2+concentration and NO concentration were observed after administration.Results The optimum combination was 10?mol/L ?-asarone+3 ?mol/L eugenol,which can decrease the concentration of intracellular Ca2+,inhibit the production of NO and increase the survival rate of PC12 cells.Conclusion The combination of effective components in Acorus tatarinowii has a better protective effect on A?25-35-induced PC12 cell injury than Acorus tatarinowii.

AIM:To explore the effect of ?-asarone on vascular endothelium and adhesion molecule expression of endothelium induced by ?-amyloid peptide from Alzheimer's disease and to estimate the injury repair.METHODS:Cultured ECV304 cells were incubated with freshly solublized A?_ 1-42 and the mixture of A?_ 1-42 and ?-asarone,the expression of three central adhesion molecules,CD106,CD62P,CE62E and Ca 2+ concentration were examined and apoptosis was recorded by Flow cytometry.Test viability of cells by MTT methods.RESULTS:The results showed that in model group and treated group,ligation of endothelial CD106,CD62P,CE62E,markers for endothelial cell activation and Ca 2+ concentration,leads to a lot of release.The livability decreased and the apoptosis increased.Further more,simultaneous treatment of ECV304 cells with ?-asarone resulted in the decrease significantly in these three adhesion molecules described above and Ca 2+ concentration as well as the livability upper and apoptosis lower.CONCLUSION:CD106,CD62P,CE62E,important inflammational factor of A?-induced endothelial injury,may be promotion of the inflammatory scade in vascular endothelial.?-asarone may protect ECV304 cell apoptosis by regulate Ca 2+ and expression of cell surface markers.

Objective To investigate the relationship between the variation of cerebrospinal fluid pulse pressure and that of intracranial perfusion pressure during the process of increasing intracranial pressure.Methods Fourteen dogs were installed epidurally with latex sacculus to establish models of increased intracranial pressure. The degree of intracranial pressure and volume could be altered by changing the volume of fluid in the sacculus. During the process, pressure transducers were arranged to monitor and record the systematic blood pressure and the variation of the pressure of cerebral ventricle and lumbar subarachnoid space.Results With the continual increasement of intracranial pressure, the cerebral perfusion pressure decreased, and the cerebrospinal fluid pulse pressure correspondingly increased. A positive linear relationship between the variation of intracranial pressure and that of cerebrospinal fluid pulse pressure and a negative linear relationship between the variation of cerebral perfusion pressure and that of cerebrospinal fluid pulse pressure were found.Conclusion During the experimental process of increased intracranial pressure, with the decrease of cerebral perfusion pressure , the cerebrospinal fluid pulse pressure increases. The relationship of variations between them shows a negative linear one. It seems that in the circumstances when the autoregulation of cerebral vessel is injured, the variations of cerebrospinal fluid pulse pressure may produce some useful information as to the changes of intracranial blood flow.

Objective To study the changes of low-frequency-component of intracranial pressure (ICP) fluctuation during intracranial hypertension. Methods 15 healthy mongrel dogs were used to make models of intracranial hypertension by arranging latex sacculus epidurally.The different amount of normal that was injected into latex sacculus led to fluctuation of ICP and alteration of intracranial volume. The pressures in ventricle and lumbar spinal canal were recorded continuously by baroceptor, and the changes of low-frequency-component of ICP fluctuation were studied by frequency-spectrum analysis. Results After increase of intracranial pressure and volume,pulse wave (M wave) with its frequency at 0.1～0.2 Hz showed continually. Conclusion Emerge of M wave may reflect some decrease of intracranial compliance and the beginning of volume compensation failure.

Objective To study the effect of automobile exhaust pollution saturation of carboxyhemoglobin (COHb) in traffic policemen. Methods 169 traffic policemen working outdoors were selected as a exposure group and 112 traffic policemen working indoors as control group in a traffic policemen detachment in Tangshan. Questionnaires and health examination were conducted in two groups. The carbon monoxide levels in the exhalation were measured in 281 traffic policemen by a micro_smokerlyzer and the corresponding saturation of carboxyhemoglobin (COHb) were read. Results The higher saturation of carboxyhemoglobin were observed in exposure group (2.30%?1.49%) compared with those (1.71%?0.99%) in control group (P

Objective To explore whether the dopamine D1 and D2 receptors were involved in pathogenic mechanism of Parkinsonian mice induced by paraquat. Methods The models of Parkinson's mice were induced by oral paraquat. The levels of dopamine D1 and D2 receptor proteins and the expression of receptor mRNAs in striatum were examined by immunohistochemistry and in situ hybridization, respectively. Results Mice treated by oral paraquat (10mg?day -1 ?kg -1 ) for four months displayed marked hypoactive behavior. The levels of dopamine D1 and D2 receptor proteins in the striatum were significantly decreased by 28% and 29%, respectively (P