Furthermore,Western blot analysis showed that the expres-sion of phosphorylated ERK was increased by silibinin,the expression of phos-phorylated p38 MAPK was decreased and total ERK,p38,JNK and phosphory-lated JNK MAPK did not change after treatment with both isoproterenol andsilibinin.Furthermore,pretreatment of cardiac myocyte with PKC,Ras and Rafinhibitors significantly

blocked ERK phosphorylation.Conclusion:Silibinin issuggested to protect isoproterenol-induced rat cardiac myocyte apoptosis byactivating the tyrosine kinase pathway,PKC 或者 and MAPK pathways.
Aim:To investigate the effect of icariin on the expression of peroxisome proliferator-activated receptor γ coactivator-1 alpha (PGC-1 α),peroxisome proliferator-activated receptor alpha (PPARα),and nuclear

respiratory factor 1 (NRF-1) oncardiomyocyte differentiation of murine embryonic stem (ES) cells in vitro.Methods:The 这个 cardiomyocytes derived from murine ES cells were verified byimmunocytochemistry using confocal laser scanning microscopy.Cardiac-specific sarcomeric proteins (ie α-actinin,troponin T) were evaluated when em-bryoid bodies (EB) were treated with icariin or retinoid acid.The expression ofPGC-1α,PPARα,and NRF-1 were analyzed using both semiquantitative RT-PCRand Western blotting in cardiomyocyte differentiation.The phosphorylation ofthe p38 mitogen-activated protein kinase (MAPK) was studied in the differentia-tion process,and its specific inhibitor SB203580 was employed to confirm thefunction of the p38 MAPK on icariin-induced cardiac differentiation.Results:The application of icariin significantly induced the cardiomyocyte differentiationof Alisertib 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 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 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.