0.05).Follow-up coronary angiography was more frequently performed in group A than in group B.Conclusion In patients with acute myocardial infarction treated with primary percutaneous coronary intervention,the transradial approach is a safe and feasible technique.With the higher rate of follow-up angiography,it was found that the incidence of MACE at 1-month follow-up and 6-month follow-up using the transradial approach was similar to transfemoral approach.Therefore,the transradial approach is expected to become the substitute approach for treatment in AMI patients.

By means of HPLC,the changes of endogenous hormones in the process of releasing dormancy in Fritillaria thunbergii Miq. seeds were determined. The results indicated that the content of GA3 had a process of increase while the content of ABA was reduced in general. The content of IAA showed a downward -plateau-upward-downward curve in the process of releasing dormancy. When the dormancy of the seeds were released attemperatures 8~10℃ and 3~5℃,changing pattern of each of the three endogenous hormones were similar,but the duration spanning each change were different.

Objective To investigate the effect of pronuciferine on apoptosis of cultured human umbilical vein endothelium cells(HUVECs) induced by angiotensin Ⅱ(AngⅡ).Methods HUVECs cell line ECV304 was cultured in vitro,pretreated with Captopril(10 ?mol/L) or pronuciferine 10,1,0.1,0.01 ?mol/L for 30 min,respectively,then treated with AngⅡ(1 ?mol/L).Cell-morphosis was observed by light microscope.Cells viability was assessed by MTT assay.Production of nitric oxide(NO),activities of total nitric oxide synthase(tNOS),and inducible nitric oxide synthase(iNOS) were measured by colorimetry.Apoptosis rate was measured by Flow Cytometer(FCM).Results AngⅡ induced typical endothelial cell apoptosis and the apoptosis rates were significantly higher than those of the control group((P

Objective To test the effect of Undaria pinnatifida soluble dietary fiber on endothelial function in hyperlipidemic rats. Method Forty rats were divided into 4 groups(n=10) :control group,hyperlipidemic model group,low dose dietary fiber-treated group(5%) ,high dose dietary fiber-treated group(10%) . After treatment for 8 w. Endothelium-dependent vasorelaxation in isolated aortic rings,the content of plasma malondialdohyde(MDA) ,nitric oxide(NO) and endothelin-1(ET-1) were determined. The protein expression of endothelial NO synthase(eNOS) was measured by Western blotting. Results Undaria pinnatifida soluble dietary fiber treatment significantly decreased MDA and ET-1 level. It also significantly improved endothelial function and plasma NO level concomitantly with unregulation of the expression of eNOS protein. Conclusion In hyperlipidemic rats Undaria pinnatifida soluble dietary fiber could improve vascular endotheliual function,which might be explained by its action to decreasing plasma ET-1 level and increased NO production.

Background and purpose:More and more evidence has showed that Grb2 binding protein-2 (Gab2) is associated with tumor invasion and metastasis. However, the relationship between Gab2 and epithelial-mesenchymal transition (EMT) in breast cancer is not clear. The aim of this study is to investigate the effect of Gab2 on EMT markers and the mechanism of Gab2 on breast cancer invasion and metastasis.Methods:Immunohistochemical methods were used to detect the expressions of Gab2, E-cadherin and vimentin in 80 cases of breast cancer tissues, and the correlations between them were analyzed. Western blot was used to detect the expression of Gab2 in breast tissues. After MDA-MB-231 cells were transfected with siRNA plasmid, wound healing assay was used to detect the invasive ability of transfected cells induced by epithelial growth factor (EGF) in vitro. Then Western blot was used to analyze the protein expressions of E-cadherin, vimentin, phosphorylated GSK-3β (p-GSK-3β) and nuclear Snail.Results:Gab2 was negatively correlated with the expression of E-cadherin and positively correlated with the expression of vimentin in breast cancer tissues (P<0.05). The expression of Gab2 in breast cancer tissues was higher than that in normal breast tissues adjacent to breast cancer. In vitro, Gab2 expression was significantly knocked down in MDA-MB-231 cells transfected with Gab2 siRNA plasmid (SiGab2/MDA-MB-231cells). Meanwhile, the invasive ability of SiGab2/MDA-MB-231cells was decreased with EGF stimulation. The expression of E-cadherin was increased in SiGab2/MDA-MB-231cells. However, the expressions of vimentin, p-GSK-3β and nuclear Snail were decreased in SiGab2/MDA-MB-231cells.Conclusion:Gab2 can promote the invasion and metastasis of breast cancer by EMT through GSK-3β/Snail signaling pathway.

Aim To investigate the protective effects of YXETNZ injection on SH-SY5 Y cells damaged by oxygen-glucose deprivation ( OGD ) , and explore its functional mechanisms. Methods After 4 h of OGD, the cells were treated with 25 mg·L-1 drugs for 1 h. Subsequently, cell viabilities were measured by cell counting kit-8 ( CCK-8 kit ) and cell apoptosis was measured by caspase-3/7 assay kit according to manu-facturer’ s instructions. Furthermore, cell death was also detected by ELISA. The levels of phospho-Akt, phospho-PKA,phospho-Bad were evaluated by western blot. Results Oxygen-glucose deprivation significant-ly decreased the cell viabilities of SH-SY5Y cells, while YXETNZ injection significantly increased cell vi-abilities, phospho-Akt, phospho-PKA and phospho-Bad. Furthermore, YXETNZ injection also reduced the activities of caspase-3/7 and cytoplasmic histone-asso-ciated-DNA-fragments contents. Conclusion Our re-searches demonstrat that YXETNZ injection shows good neuroprotective effects on SH-SY5 Y cells after oxygen-glucose deprivation. The underlying mechanisms may be associated with activation of PI3 K/Akt/Bad/caspase-3/7 , cAMP/PKA/Bad/caspase-3/7 signaling pathway.

Aim To investigate the protective effects of Diterpene Ginkgolides Meglumine Injection(DGMI)on SY5 Y cells damaged by oxygen-glucose deprivation and its functional mechanisms.Methods After 4 h of OGD,the cells were treated with 25 mg·L-1 drugs for 1 h.Subsequently,cell viabilities were measured by cell counting kit-8(CCK-8 kit)and cell apoptosis was measured by flow cytometric analysis.Furthermore, the mitochondrial membrane potential was detected by rhodamine123 staining.The levels of phospho-p38, phospho-p53,Bcl-2,Bax and cleaved caspase-9/3 were evaluated by western blot.Results DGMI signif-icantly increased the cell viabilities of SY5 Y cells dam-aged by OGD,and reduced OGD-elicited dissipation of mitochondrial membrane potential and cell apoptosis. Furthermore,DGMI also reduced p-p38,p-p53,Bax/Bcl-2 ratio,cleaved caspase-9 and cleaved caspase-3. Conclusion DGMI shows good neuroprotective effects on SY5 Y cells after oxygen-glucose deprivation.The underlying mechanisms may be associated with the sup-pression of p38/p53/Bcl-2 /caspase-9/caspase-3 sig-naling pathway.

OBJECTIVE To investigate the protective effects and mechanism of diterpene ginkgolides meglumine injection (DGMI) against oxidative stress induced by oxygen-glucose deprivation (OGD) in SH-SY5Y cells. METHODS SH-SY5Y cells were divided into five groups: normal control, model control (OGD group) and drug(25 mg · L- 1) administration groups including DGMI group, extract of ginkgo biloba leaves injection group (EGBLI) and lactones ginkgo biloba injection group (LGBI). The cells suffered from oxygen-glucose deprivation (OGD) for 4 h, followed by reoxygenation with drugs for 6 h. Then, cell viabilities were detect using CCK-8 assays, reactive oxygen species (ROS) levels using fluorescence probe DCFH-DA and superoxide dismutase (SOD) activities using WST-1 test. Western blotting was used to detected protein levels of hemeoxygenase-1(HO-1), NAD(P)H, quinone oxidore?ductase l (Nqo1), protein kinase B (Akt), phosphorylated Akt (p-Akt), nuclear factor-E2-related factor2 (Nrf2) and phosphorylated Nrf2 (p-Nrf2). The cells were induced by OGD for 4 h, followed by reoxygen?ation and DGMI for 1 h, combined with different concentrations of PI3K inhibitor (LY294002) (at the final concentration of 12.5, 25 and 50 μmol · L-1) before the protein levels of AKT, p-AKT, Nrf2 and p-Nrf2 were detected by Western blotting. RESULTS SH-SY5Y cells induced by OGD for 4 h resulted in an increase in ROS(P<0.01), but a decrease in cell viabilities(P<0.01), SOD activities(P<0.01), and antioxidant protein levels ( Akt, p-Akt, Nrf2, p-Nrf2, HO-1 and Nqo1) (P<0.01). Compared with OGD group, treatment with reoxygenation and drugs (DGMI,EGBLI and LGBI respectively) for 6 h resulted in a decrease in ROS (P<0.01), but an increase in cell viabilities, SOD activities and antioxidant protein levels of p-Nrf2, HO-1, Nqo1 and p-Akt(P<0.05,P<0.01). DGMI group showed the best efficiently. Moreover, after OGD for 4 h, compared with DGMI group, combining reoxygenation and DGMI with LY294002 for 1 h resulted in a concentration-dependent inhibition of the protein levels of p-AKT and p-Nrf2(P<0.01). CONCLUSION DGMI 25 mg · L-1 can inhibit oxidative stress in SH-SY5Y cells induced by OGD by increasing the activity and expression of Nrf2 through PI3K/Akt pathway, which may be one of the mechanisms by which DGMI protects neurons from stroke.

Objective The purpose of this study was to establish a rat model of thromboembolism for the study of hemorrhag -ic transformation after intravenous thrombolysis with the recombinant tissue plasminogen activator ( rtPA) . Methods Sixty Sprague-Dawley rats were randomly divided into a sham operation , a cerebral embolism, and an rtPA group.Thrombus was prepared in vitro with the rat femoral artery blood and injected into the internal carotid artery of the rats in the cerebral embolism and rtPA groups to es -tablish a model of embolic focal cerebral ischemia , while the animals of the sham operation group injected with BSA .Five hours later , the rats in the rtPA group received rtPA and those in the cerebral embol-ism and sham operation groups the injection of isotonic saline solu-tion.At 24 hours after embolus injection , the neurological deficit score was obtained .The rats were sacrificed after cardiac perfusion and their brains removed for triphenyltetrazolium chloride staining , assessment of the infarct volume and cerebral edema , and calculation of the hemorrhage volume by spectrophotometric hemoglobin assay . Results The hemorrhage volume was significantly higher in the rtPA than in the cerebral embolism group ([17.55 ±2.20] μL vs [3.82 ±0.86] μL, P<0.01), but there were no statistically significant differences between the two groups in the infarct volume ([29.29 ±4.204] %vs [27.89 ±3.91] %, P=0.810), cerebral edema ([12.43 ±1.66] % vs [7.13 ±2.04] %,P=0.063 2), and neurological deficit score (3.35 ±0.27 vs 2.80 ±0.28, P=0.174). Conclusion The rat model of thromboembolism, with a high stability and reproducibility , can be used for the pathogenesis-related studies of hemorrhagic transformation after thromboly-sis with rtPA.