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.

Objective To observe the effect of β-asarone on the proliferation, cycle, apoptosis and migration of tumor cells A549, PC3, and PC9-R, thus to provide experimental basis for the application of β-asarone to the treatment of cancer. Methods After A549, PC3, and PC9-R were cultured with different concentrations ofβ-asarone for 24 h, 48 h, and 72 h respectively, CCK-8 was used to detect the optical density (D) of cell proliferation, and then the cell proliferation rate was calculated. The flow cytometry was used to measure the cell DNA cycle and cell apoptosis, and Transwell Chambers were used to detect the cell migration. Results After treatment with different concentrations of β-asarone for 24 h, 48 h, and 72 h respectively, the growth of A549, PC3, and PC9-R showed declining trend in concentration- and time-dependent manner. The proportion of A549, PC3, and PC9-R at G0/G1 phase was increased, the proportion of the three kinds of cells at S phase and the proliferation indexes were declined, the apoptotic rate of A549, PC3, and PC9-R was increased, and the migration of A549, PC3, and PC9-R was reduced (P<0.05 or P<0.01 compared with those of the normal control group). Conclusion β-asarone has certain effects on suppressing proliferation, blocking G0/G1 phase developing into S phrase, inhibiting DNA synthesis, promoting the apoptosis, and inhibiting the migration of A549, PC3 and PC9-R.

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 whether folate deficiency cause high expression level of interferon gamma (IFN-γ) resulted from IFN-γ gene ( IFNG) hypomethylation and then promote the pathogenesis and development of ulcerative colitis (UC ) in a dextran sulfate sodium (DSS )-induced experimental colitis model in mice .Methods A total of 24 female BALB/c mice were divided into four groups ,six mice in each group , including folate deficient/DSS+ group , standard diet/DSS+ group , standard diet/DSS - group and folate deficient/DSS- group .At the beginning of the sixth week since fed , the mice of model groups were treated with 5% DSS to establish experimental colitis .By the end of the sixth week ,disease activity index (DAI) of colitis and histological changes were evaluated .The folate level of peripheral blood serum of mice were detected by enzyme-linked immunosorbent assay (ELISA ) . The expression of IFN-γ in colonic mucosa of mice was examined by immunohistochemistry . The methylation level of CpG island in the promoter region of IFNG was determined by methylation specific polymerase chain reaction (MSP) .The t test was used for measurement data .Chi square test was performed for comparison between groups of count data . Spearman correlation analysis was used for correlation analysis .Results The folate levels of peripheral blood serum of folate deficiency/DSS+ group and folate deficiency/DSS- group ((2 .70 ± 0 .19) and (2 .80 ± 0 .25)μg/L) were significantly lower than those of standard diet/DSS+ group and standard diet/DSS- group ((13 .62 ± 0 .38 ) and (13 .52 ± 0 .77)μg/L ,t= -63 .33、32 .27 ,both P< 0 .05) ,resepectively .The expression of IFN-γ in colonic mucosa of folate deficiency/DSS+ group and standard diet/DSS+ group were significantly higher than those of folate deficiency/DSS- group and standard diet/DSS- group (χ2 = 22 .18 ,P< 0 .05 ) . And the expression of IFN-γ in colonic mucosa of folate deficiency/DSS+ group was also higher than that of standard diet/DSS+ group (χ2 = 12 .00 ,P< 0 .05) .The expression level of IFN-γ of folate deficiency/DSS+ group and standard diet/DSS+ group was positively correlated with (r=0 .998、0 .953 ,both P<0 .01) .The folate levels of peripheral blood serum of folate deficiency/DSS+ group was negatively correlated with IFN-γexpression level and DAI (r= -0 .880 and -0 .926 ,both P<0 .05) .No abnormal methylation was detected in IFNG promoter CpG island in colonic mucosa tissues of mice of each group . Conclusion In the mice model of DSS induced acute experimental colitis ,folate deficiency may increace the expression of inflammatory factor IFN-γand enhance the inflammation activity of colonic mucosa .

Objective To explore changes of expression of pro-and anti-inflammatory cytokines in the hippocam-pus of Aβ1-42-induced Alzheimer’s disease (AD) rat model. Methods Twenty-four SD rats were divided into control group, PBS group (PBS was injected into CA1 area of hippocampus) and AD model group (Aβ1-42 was injected into CA1 area of hip-pocampus). The escape latency was evaluated by Morris water maze in three groups. Nissl staining was used to detect the le-sions of hippocampal CA1 neurons. Levels of amyloid precursor protein (APP) and protein phosphatase 2A (PP2A) in hippo-campus were measured by Western blot analysis. Real-time PCR was employed to examine the expressions of pro-inflamma-tory cytokines, including interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α) and interferon-γ (IFN-γ), and the mRNA expressions of anti-inflammatory cytokines, including IL-4, IL-10 and transforming growth factor-β(TGF-β). Re-sults Rats subjected to Aβ1-42 injection in bilateral hippocampus led to a ability reduction of learning and memory, a loss of neurons in hippocampus and an increase in the expression of APP, and a decrease in PP2A expression in the hippocampus. In AD hippocampus, The mRNA expressions of the pro-inflammatory mediator, IL-1β, TNF-αand IFN-γ, were significant-ly up-regulated, but the expressions of the anti-inflammatory cytokines, IL-4, IL-10 and TGF-β, were markedly down-reg-ulated in AD group compared with those of control and PBS groups. Conclusion The pro-inflammatory/anti-inflammatory imbalance induced neuro-inflammation in AD rats, which was involved in pathogenesis of AD.

Objective To study the expression of HGF , RAGE in placentas of patients with gestational diabetes mellitus and its relationship with maternal and neonatal prognosis .Methods The complete clinical datas of late pregnancy,GDM treated group 40 cases,GDM untreated group 23 cases,the control group 30 cases.Immunohisto-chemical method was used to detect HGF and RAGE in the placentas of three groups ,the maternal and neonatal prog-nosis were recorded.Results In GDM untreated group,GDM treated group and the controlled group placenta ,HGF and RAGE expressed.The expression of HGF was gradually increased ,and any comparative differences between two groups were statistically significant ( F =7.56, P <0.05 );the expression of RAGE in placentas was gradually declined ,the differences among the control group and GDM untreated ,GDM treated group were statistically significant (F=11.62,P<0.05).The rates of maternal and neonatal complications in the GDM untreated group were signifi-cantly higher than that of the GDM treated group and the control group (χ2 =7.34,13.21,9.75,6.67,15.23, 12.53,all P<0.05).Conclusion HGF and RAGE may participate in the occurrence and development of GDM and maternal and neonatal prognosis closely ,regular treatment can improve the prognosis of mothers and infants .

Objective To observe the protective effect of?-asarone,the active components from Rhizoma Acori Tarinowii,on human umbilical venous endothelial cell strain ECV304 injury induced by oxidized low-density lipoprotein(ox-LDL)and to investigate its influence on proliferation of vascular smooth muscle cells(VSMC). Methods The well-grown ECV304 cells were randomized into 5 groups:normal group,control group,high-, middle-and low-dose?-asarone groups.Except the normal group,ECV in the other groups were co-cultured with ox-LDL 25?g/mL,and the?-asarone groups were additionally with?-asarone 30,15 and 7.5?g/mL added respectively.Flow cytometry was used to detect the cell apoptotic rate and the mitochondrial membrane potential (MMP)of ECV304 as well as the proliferation index and the DNA content in different cell phases of VSMC. Results In the model group,the apoptotic rate of ECV was increased,MMP was decreased,and VSMC proliferation was promoted(P

AIM: To observe the enhancement of ginsen stem leaves (GSL) to the antitumor effect of 5 FU in mice inoculated S180. METHODS: The different combinations of GSL and 5 FU were used to examine the inhibition rates of tumor growth in KM mice inoculated S180. RESULTS: The combination of GSL (15 mg?kg -1 ) and 5 FU (1.5 mg?kg -1 ) obtained 26.90% of inhibition rates of tumor growth (P