Results:The application of icariin significantly

induced the cardiomyocyte differentiationof EB as indicated by the promoted expression of α-actinin and troponin T.Theexpression of PGC-1α,PPARα,and NRF-1 increased coincidently in early differ-entiation and the increase was dose-dependently Epigenetics抑制剂 upregulated by icariin treatment.The phosphorylation of the p38 MAPK peaked on d 6 and decreased after d 8,andthe activation was further enhanced and prolonged when the EB were subjectedto icariin,which was concurrent with the elevation of PGC-1α,PPARα,and NRF-1.Moreover,the inhibition of the p38 MAPK pathway by SB203580 efficientlyabolished icariin-stimulated cardiomyocyte differentiation and resulted 点击此处 in the cap-ture of the upregulation of PGC-1α,PPARα,and NRF-1.Conclusion:Takentogether,icariin promoted the expression of PGC-1α,PPARα,and NRF-1 duringcardiomyocyte differentiation of murine ES cells in vitro and the effect was partlyresponsible

for the activation of the p38 MAPK.
Aim:To investigate the effect of aspirin on the apoptosis of cultured bovineaortic endothelial cells(BAEC)and the signal pathways involved in this process.Methods:BAEC were cultured and passaged in Dulbecco’s modified Eagle’smedium culture medium.Morphologic changes and quantification of apoptoticcells were determined using fluorescence microscope after staining the cells withHoechst 33258.Cell viability was measured selleck screening library by 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide(MTT)method.DNA fragmentation was visualizedby agarose gel electrophoresis.Phospho-p38 mitogen-activated protein kinase(MAPK)expression was detected by Western blotting.Results:Aspirin at lowconcentrations from 1×10~(-10)mol/L to 1×10~(-8)mol/L decreased the apoptosis andp38 MAPK pbosphorylation

induced by H_2O_2 in BAEC,while high doses of aspi-rin(1×10~(-7)-1×10~(-4)mol/L)induced typical apoptotic changes in BAEC and stimu-lated the expression of phospho-p38 MAPK in a concentration-dependent manner.SB203580,a specific p38 MAPK inhibitor,blocked such effects.Conclusion:Aspirin exhibits a biphasic effect on the apoptosis in BAEC,reducing apoptosisat low concentration and inducing apoptosis at high concentration,p38 MAPKmay be an important signal molecule mediating the effects of aspirin.
Aim:To characterize the molecular mechanisms of nitrofen-induced pulmonaryhypoplasia.Methods:After administration of nitrofen to cultured type Ⅱ A549pneumocytes,cell proliferation and DNA synthesis were investigated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide colorimetry,colony forma-tion assay,flow cytometry and[~3H]-thymidine incorporation assay.Apoptosiswas measured by terminal transferase-mediated dUTP nick-end-labeling,acridineorange-ethidium bromide staining and flow cytometry.