In contrast, neither NAC nor DTT alone BMS-354825 Src inhibitor an obvious effect on platelet function apoptosis. Taken together, these data show that ROS plays a role The key cisplatin-induced Blutpl Ttchen apoptosis. R The Ca2 in cisplatin-induced apoptosis has been reported that a hte obtained Intracellular Re Ca2 cisplatin concentrations in 224 enucleated cells and a durchl SSIGE membrane Ca2 chelator BAPTA’m obviously inhibited caspase 3 activation by cisplatin in enucleated cells induced 224 . Thus, if Ca2 is involved in cisplatin-induced apoptosis are examined in this study. As shown in Fig. 8, was the intracellular Re Ca2 concentration significantly in platelets with cisplatin, which was prevented by BAPTA AM treatment increased Ht. In addition, chelation of Ca 2 apparently blocks the cisplatin-induced ERK activation, PS exposure and caspase 3 activation, suggesting that Ca 2 in the apoptosis-induced Pl Ttchen cisplatin involved. Cisplatin does not induce platelet activation PS exposure is the hallmark of platelet activation. Thus, when bound cisplatin platelet activation also investigated. Blutpl ttchen Were incubated with cisplatin of the vehicle and A23187 as negative and positive controls and then were subjected to flow cytometric analysis using the Recogn t SZ51 specifically expressed Pl Ttchenoberfl Surface P-selectin flowing S shown in FIG. 9A and B has not cisplatin L Sen the surface chenexpression Of P-selectin obviously also displays. 9C shows that no CAP binding observed in cisplatin treated Blutpl buy Streptozotocin Ttchen. In comparison, PAC-1 positive platelets were detected in the contr The A23187 treated. Taken together, these data show that cisplatin induces no Blutpl Ttchen activation. Cisplatin cisplatin Changed platelet function has been reported that Thrombozytenreaktivit t improve with non-aggregating concentrations of agonists, however, it is shown that cisplatin prevented.
Blutpl Ttchen agonist-induced aggregation. In this study, the PI Ttchenaggregation by ristocetin / VWF-induced or thrombin significantly in washed platelets and PRP treated with cisplatin has been dropped before. Furthermore, as shown in Fig. 9E and F, both the number of adh Pensions platelets and the Cathedral Ne of Blutpl Ttchenmembran spreading on VWF matrix were significantly reduced. Taken together, these data suggest that cisplatin VER Changed platelet function. The discussion here pr Sentierten data show that apoptosis of cisplatin Blutpl ttchen Induced by the ERK signaling pathway. Cisplatin does not induce platelet activation, w While he VER Obviously changed platelet function. The conclusion that cisplatin induces apoptosis of Blutpl ttchen by the ERK pathway is supported by various information: cisplatin induces increased expression of pro apoptotic proteins hte, and decreased expression of anti-apoptotic. The activation and mitochondrial translocation of Bax were induced in platelets Checkpoint treated with cisplatin. Cisplatin dose- Ngig depolarization caused Δ Ψ m. Cisplatin induces the activation of caspases 3 and PS exposure, which were significantly fmk by caspase-3-specific inhibitor Z-DEVD. Cisplatin activated ERK in a dose-dependent Ngigen manner and blockade of ERK PD98059 or U0126 prevents cisplatin-induced Blutpl Ttchen-apoptotic cascade.