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.

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

Objective To observe the effects of MPP+ on the expression of inhibin, activin and its receptor ⅡA and cell ability in PC12 cells of rats.Methods The changes of expression of activin?A, activin?B, inhibin? and receptorⅡA mRNAs were assayed by RT-PCR, the change of cell viability was detect by tyrpan blue exclusion method in cultured PC12 cells at 3 h,6 h,12 h,24 h after MPP+ was added and compared with control groups.Results The expression of activin?A, activin?B and activin receptorⅡA mRNAs in PC12 cells were down-regulated significantly after MPP+ administrated at every time point while the expression of inhibin? mRNA remained unchanged. The cell viability decreased at the points of 12 h and 24 h after MPP+ administrated.Conclusion MPP+ may cause the injury of PC12 cells by downregulating the expression of activin and its receptor.

Objective To evaluate the protective role of bone marrow stromal cells (BMSCs) to lactacystin-Parkinson's disease (PD) rats.Methods BMSCs were obtained from adult male SD rats and were expanded, isolated and purified. BMSCs were harvested from 4 to 6 passage and used for transplantation. PD rats that expressed Lewy body and presented lateral rotation were made by injecting 8?g lactacystin into one side of substantia nigra compact part of rat with stereotaxic technique. The rats were transplanted with BMSCs labelled by Brdu by stereotaxic unilateral injection into striatum and transplanted with normal saline as control. The behavior changes of rats and the expression of BDNF, migration, differentiation of BMSCs were examined.Results 71.43% of the rats displayed significant improvement of contralateral behavior after BMSCs transplantation, however there was no change in control group. BMSCs were found in several areas of the brain including striatum, corpus callosum and contralateral cortex. The implanted BMSCs expressed BDNF but no tyrosine hydroxylase.Conclusion BMSCs may play a neuroprotective role in lactacystin-PD rats by secreting BDNF.

Objective To set up the Parkinson's disease(PD)rat model with pathologic characteristic of Lewy body in nigral cells.Methods SD rats were injected respectively with 8 mg Lactacystin(Lactacystin group),sodium saline(NS group)and 12 mg 6-OHDA(6-OHDA group)by stereotaxic unilateral injection into the pars compacta of substantia nigral.The spontaneous and apomorphine-induced contralateral behaviors of rats were observed.The changes of midbrain histology were viewed by microscope;expression of ?-synuclein and tyrosine hydroxylase(TH)positive cells were investigated by immunohistochemistry.The contents of dopamine and homovanillic acid in striatum were determined.Results Rats of NS group did not display abnormal behavior.The animals treated with Lactacystin developed progressively bradykinesia,hypokinesia,tremor,contralateral head tilting,and displayed apomorphine-induced contralateral rotation behavior;3 weeks later the number of TH positive cells were decreased by 83.29% compared with NS group(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.