[Mechanism of Mitochondria-mediated Pathway in the Platelet Apoptosis Resulted from Immune Bone Marrow Failure].

OBJECTIVE: To explore the mechamisms of mitochondria-mediated pathway in apoptosis of platelets resulted from in immune induced bone marrow failure. METHODS: Thirty C57BL/6 mice were randomly divided into 3 groups (10 mice in each group): normal group, model group, cyclosporine A(CsA) group. Mouse model of immune bone marrow failure were established. After mouse model was successfully established, the mice in normal group and model group were given saline orally, the mice in CsA group was treated with CsA orally. Blood routine examination of mice in each group was performed by automatic blood cell analyzer; the mitochondrial membrane potential(ΔΨm), cytochrome C(Cyt C), phosphatidylserine (PS), Ca2+ were measured by flow cytometry; expression of BAX, BAK, caspase-3, caspase-8, caspase-9 was detected by using Western blot method, the changes of bone marrow platelet ultrastructure were observed under transmission electron microscope. RESULTS: Compared with normal group, the platelet count of model group decreased significantly, while the level of ΔΨm, caspase-3, caspase-8, caspase-9 significantly decreased, the level of Cyt C, PS, Ca2+, BAX, BAK increased significantly (P<0.05). Compared with the model group, the platelet count of CsA group increased obviously, while the level of ΔΨm, caspase-3, caspase-8, caspase-9 of CsA group increased significantly, the level of Cyt C, PS, Ca2+, BAX, BAK of CsA group decreased significantly (P<0.05). Electron microscopy showed that compared with the model group, platelet damage in CsA group were alleviated. CONCLUSION: mitochondrial pathway plays an important role in the reduction of platelet resulted from immune bone marrow failure.

rmhTNF-α combined with cisplatin inhibits proliferation of A549 cell line in vitro.

OBJECTIVE: To explore the inhibitory effect of recombinant mutant human tumor necrosis factor-Α (rmhTNF-Α) in combination with cisplatin on human lung adenocarcinoma cell line A549. METHODS: Human lung adenocarcinoma cell line A549 was treated with varying concentrations of rmhTNF-Α (0.38, 0.75, 1.50, 6.00 and 12.00 IU/ml) or cisplatin (3.91, 7.81, 15.63, 31.25 and 62.50 Μg/ml) for 24 hours. Viable cell number was analyzed by using crystal violet staining. The inhibitory rates of A549 cells growth by the two drugs were calculated. For analyzing whether there was a synergistic effect of rmhTNF-Α with cisplatin, A549 cells were treated with 0.75 IU/ml rmhTNF-Α and increased concentrations of cisplatin. RESULTS: rmhTNF-Α or cisplatin inhibited the growth of A549 cell lines in a dose-dependent manner. The inhibitory effect of rmhTNF-Α combined with cisplatin was significantly greater than cisplatin alone at the same concentration (all P<0.01). CONCLUSION: rmhTNF-Α combined with cisplatin might have synergistic inhibitory effect on human lung adenocarcinoma cell line A549.