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AIM: To investigate the effects of celecoxib on viability, apoptosis and autophagy in acute myeloid leukemia (AML) cell lines HL-60 and HL-60A. METHODS: The HL-60 cells and HL-60A cells were cultured with various concentrations (0, 20, 40, 60, 80 and 100 μmol/L) of celecoxib. The inhibitory effect of celecoxib on the cell viability was evaluated by MTT assay. Apoptosis was analyzed by Annexin-V/PI staining. Apoptosis-related and autophagy-related proteins were determined by Western blot. RESULTS: IC50 of celecoxib were 49.4 μmol/L, 32.0 μmol/L and 25.1 μmol/L for HL-60 cells treated with celecoxib for 24 h, 48 h and 72 h, respectively. For HL-60A cells, the corresponding IC50 were 69.1 μmol/L, 42.5 μmol/L and 29.6 μmol/L, respectively. The results of flow cytometry analysis showed the proportions of Annexin-Ⅴ+ PI-, Annexin-Ⅴ+ PI+ and Annexin-Ⅴ-PI+ cells were increased in the HL-60 cells, and those of Annexin-Ⅴ+PI- and Annexin-Ⅴ+ PI+ cells were increased in the HL-60A cells treated with celecoxib for 24 h. After treated with celecoxib, the induction of apoptosis was observed, the apoptosis-related proteins cleaved caspase-3 and cleaved PARP were upregulated, the autophagy-related proteins LC3 II and P62 were both increased, and mTOR, p-mTOR, 4-EBP and p-4-EBP were not changed, indicating that celecoxib inhibited autophagy in the AML cells without the mTOR pathway involvement. CONCLUSION: Celecoxib inhibits the viability of HL-60 cells and HL-60A cells in a time-and dose-dependent manner by its effects of inducing apoptosis and necrosis. Celecoxib inhibits mTOR-independent autophagy in AML cells, indicating a possible way of using celecoxib for enhancing the antitumor activity of therapeutic agents to induce cytoprotective autophagy in the AML cells.  相似文献   
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AIM: To investigate the effects of celecoxib, a selective cyclooxygenase-2 inhibitor, on antioxidative capability and apoptosis of cardiac myocytes after myocardial infarction. METHODS: 24 New Zealand rabbits were divided into three groups randomly (8 in each group): sham-operated group (sham group), myocardial infarction group (MI group), celecoxib group (Cele group, 10 mg kg-1·d-1, qd, with the drugs gastric gavage for six weeks). The NO concentration, total antioxidative capability (T-AOC), the activity of constitutive nitric oxide synthase (cNOS) and inducible NOS (iNOS) in cardiac tissue homogenate, adjacent to the infracted area, were detected. The pathological changes were observed by light microscope and electron microscopy. The expressions of Bcl-2 and Bax protein in myocytes were observed using immunohistochemistry, and the degree of apoptosis were examined by TUNEL. RESULTS: Cardiac tissue in MI group presented interstitial edema, fibroplastic proliferation, inflammatory cellular infiltration, and vacuolar degeneration in cardiac myocytes. The results of electron microscopy showed that myocytes presented more changes caused by ischemic injury: widened interspace of myofibril, disordered myofibrillae, focal lysis of myofilament, ectasia of sarcoplasmic reticulum. In Cele group, the pathological changes were light, the NO-2/ NO-3 concentration, the activity of iNOS were lower (P<0.05), while the activity of cNOS and T-AOC were higher (P<0.05) than those in MI group. The expression rate of Bcl-2 protein in Cele group was higher than that in MI group, while the Bax was lower (P<0.01). The number of apoptotic myocytes was lower than that in MI group (P<0.01).CONCLUSION: Celecoxib decreases the number of apoptotic cardiomyocytes and increases the antioxidative capability after myocardial infarction.  相似文献   
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AIM:To investigate whether SC58125 synergizes with TNF-α to induce HT-29 cell apoptosis and study the possible molecular mechanism. METHODS:By using MTT,Hoechst 33342 staining and agarose gel electrophoresis,the effect of SC58125/TNF-α on the proliferation and apoptosis of HT-29 cell line was examined. The activity of caspase-3,the expression of IκBα,the phosphorylation level of IκBα,and the activation of NF-κB were measured after treatment with SC58125 by electrophoretic mobility shift assay and Western blotting.RESULTS:Both SC58125 and TNF-α exhibited cytotoxicity. The combination of the two reagents significantly reduced HT-29 cell viability in a dose-dependent manner. SC58125 and TNF-α co-treated cells showed induced nuclear condensation and fragmentation,and led to oligonucleosomal cleavage of genomic DNA,which was accompanied by the induction of caspase activity. IκBα levels were substantially decreased by the treatment of TNF-α. The degradation of IκBα was almost completely inhibited when SC58125 was added. NF-κB was activated in HT-29 cells after treatment with TNF-α,whereas pretreatment of HT-29 cells with SC58125 for 2 h,TNF-α induced NF-κB DNA binding was profoundly suppressed. CONCLUSION:SC58125 synergizes with TNF-α to inhibit cell growth and induces apoptosis in HT-29 cells,which may be mediated by activating caspase-3 and preventing degradation of IκBα.  相似文献   
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