E process. Thus, additionally Tzlich HDAC inhibition to the frequency of the monofunctional adducts, the F Ability of these L Emissions escape repair and / or by preventing replicative passCisplatin is one of the h Ufigsten used anti-tumor agents of compounds based on platinum. Cisplatin-based chemotherapy, usually by several toxicity As nephrotoxicity th t, Ototoxizit t and peripheral neuropathy accompanied. In particular, cisplatin liable thrombocytopenia, and platelet counts significantly in rats with acute doses of treated patients reduced S of cisplatin. Although it was best Firmed that cisplatin induces apoptosis in various types of solid tumors and in tumor cells do not, it remains unclear whether cisplatin can induce Blutpl Ttchen apoptosis. The apoptosis of platelets by regulating apoptotic pro, down-regulation of the fight against apoptotic proteins, activation and mitochondrial translocation of Bax, mitochondrial depolarization inner transmembrane potential, caspase activation and exposure of 3 phosphatidylserine occurs, h Frequently in vivo ttchen and in vitro in response to chemical or physiological agonists, shear stress, or the storage of Blutpl. Although apoptosis of platelets and platelet activation shares several morphological Bcr-Abl inhibition and biochemical characteristics, the signal transduction pathways to these two different Ph Phenomena. Cisplatin appears to Thrombozytenreaktivit t in concentrations of aggregation agonists, such as collagen and arachidonic improve Sodium acid by a mechanism in which arachidonic Acid metabolism is involved. However, it is also shown that cisplatin inhibitory effect on concentrations of ADP and Blutpl Ttchen shows induced by thrombin. Thus, the effect of cisplatin on Blutpl Ttchen activation is not elucidated rt.
Extracellular regulated kinase Res signal was reported to play an r The most important cytokines in apoptosis with phorbol ester, and NH 2-terminal kinase c was in June and p38 kinase is also induced apoptosis by stress signals is emphasized especially UV radiation and hyperosmotic. However, the r Of ERK in cisplatin-induced apoptosis controversial. The activation of ERK plays a role The key in the induction of apoptosis in several types of cells treated with cisplatin. Conversely, tr Activation of ERK gt on the chances of survival of ovarian cancer cells, the cisplatin. Furthermore, the activation of ERK in Blutpl Ttchen activation is triggered by several agonists most. Therefore analyzed SB203580 or 37 for 5 min or SP600125 for 10 min at 37 and then were treatedwith cisplatin at 37 for 30 minutes and byWestern blot. The DMSO concentration in each sample not more than 0.1%. For the isolation and analysis of Blutpl Ttchen mitochondrial fraction, min, the platelets before with cisplatin at 37 for 30 min and then were then incubated in the mitochondrial isolation buffer A for 2, buffer B for 5 minutes, and Cell Cycle/Checkpoint buffer C for 5 followed, by centrifugation. The whichever type walls The Blutpl Ttchen lysates were further centrifuged at 12,000 g for 20 min. The pellets, the mitochondria were washed once with buffer C and then in a lysis buffer for 30 min Gel Hrs, then were centrifuged at 12,000 g for 5 min. The samples were analyzed by SDS-PAGE and Western blot. Confocal microscopy of washed platelets.