01,P
Aim:To investigate the mechanism of silibinin-protected isoproterenol-inducedapoptosis in rat cardiac myocytes.Methods:The viability of rat cardiac myocyteswas measured by MTT method.The apoptotic ratio was measured by terminaldeoxynucleotidyl transferase-mediated dUTP nick end-labeling.Protein kinase C(PKC) activity assay was carried out according to the instructions of the PepTagnon-radioactive protein kinase C assay kit.Western blot analysis was used toevaluate the level of Ras,Raf-1 没有 and mitogen-activated protein kinase (MAPK)expression.Results:The protective effects of silibinin were significantly sup-pressed by inhibitors,including

genistein,manumycin A and GW5074 [inhibitorsfor protein tyrosine kinases (PTK),Ras and Raf-1,respectively].The Cilengitide exposure ofrat cardiac myocytes to isoproterenol alone caused decreased PKC activity,whichwas prevented by pretreatment with silibinin dose-dependently.Simultaneously,the increased expression of Ras and Raf-1 activated by silibinin were blocked bythe PKC inhibitor,stauroporine.In addition,the extracellularly responsive kinase(ERK) inhibitor,PD98059,suppressed silibinin-protected apoptosis,whereas thep38 MAPK inhibitor,SB203580,protected cardiac myocytes from isoproterenol-induced injury,and the c-Jun N-terminal

kinase (JNK) inhibitor,SP600125 had noprotective effects.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 Saracatinib细胞系 issuggested to protect isoproterenol-induced rat cardiac myocyte apoptosis byactivating the tyrosine kinase pathway,PKC 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 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.