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Study on the function and mechanism of atorvastatin in regulating leukemic cell apoptosis by the PI3K/Akt pathway |pdf=|usr=}}{{26064227}} gab.com Text Study on the function and mechanism of atorvastatin in regulating leukemic cell apoptosis by the PI3K/Akt pathway JO: Int J Clin Exp Med http://www.kidney.de/pget.php?&tw=1&pmid=26064227 #FOAvip Objective: To investigate the effects of atorvastatin on the proliferation and apoptosis of leukemic cell lines (Jurkat, K562 and HL-60), and expore the function of TLR4/MYD88/NF-?B and PI3K/AKT signal pathway in this process. Methods: Cells in logarithmic growth phase were divided into negative control group and experimental group (cells were treated with atorvastatin with intervention concentrations of 1, 5 and 10 ?mol/L respectively) and cultured for 24 hours. Changes in apoptosis and cell cycle of leukemic cells were detected utilizing the Flow Cytometry. Changes in the expression of TLR4/MYD88/NF-?B and PI3K/AKT signal pathway related genes were detected utilizing Real-time PCR and Western Blot method. Results: Atorvastatin inhibit proliferation and induce apoptosis in K562, HL-60 and Jurkat cells in a dose-dependent manner. K562, HL-60 and Jurkat cells in G0/G1 phase increased and that in S phase decreased after being treated with atorvastatin for 24 hours compared with that in control group, suggesting that the atorvastatin can retard the three cells in the G0/G1 phase. The study find that the basal expressions of TLR4, MYD88 and NF-?B gene in K562, HL-60 and Jurkat cells are obviously down-regulated in a dose-dependent manner after being treated with atorvastatin with different concentrations. This down-regulation action of atorvastatin to the expression of the TLR4, MYD88 and NF-?B gene becomes more obvious with the increase of the drug level. In addition, the PI3K, AKT and their phosphorylation levels in the above cells down-regulate obviously in a dose-dependent manner after being treated with atorvastatin. This down-regulation action of atorvastatin to the PI3K, AKT and their phosphorylation levels become more obvious with the increase of the drug level. Conclusions: Atorvastatin can inhibit proliferation and induce apoptosis in leukemia cells, which may be associated with the regulation of atorvastatin to the TLR4/MYD88/PI3K/AKT/NF-?B signaling pathway. Twit Text FOAVip Study on the function and mechanism of atorvastatin in regulating leukemic cell apoptosis by the PI3K/Akt pathway ????Int J Clin Exp Med http://www.kidney.de/pget.php?&tw=1&pmid=26064227 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26064227 #FOAvip English Wikipedia <ref>{{Cite pmid|26064227}}</ref> Study on the function and mechanism of atorvastatin in regulating leukemic cell apoptosis by the PI3K/Akt pathway #MMPMID26064227 Liu M; Tang R; Jiang Y Int J Clin Exp Med 2015[]; 8 (3): 3371-80 PMID26064227show ga Objective: To investigate the effects of atorvastatin on the proliferation and apoptosis of leukemic cell lines (Jurkat, K562 and HL-60), and expore the function of TLR4/MYD88/NF-?B and PI3K/AKT signal pathway in this process. Methods: Cells in logarithmic growth phase were divided into negative control group and experimental group (cells were treated with atorvastatin with intervention concentrations of 1, 5 and 10 ?mol/L respectively) and cultured for 24 hours. Changes in apoptosis and cell cycle of leukemic cells were detected utilizing the Flow Cytometry. Changes in the expression of TLR4/MYD88/NF-?B and PI3K/AKT signal pathway related genes were detected utilizing Real-time PCR and Western Blot method. Results: Atorvastatin inhibit proliferation and induce apoptosis in K562, HL-60 and Jurkat cells in a dose-dependent manner. K562, HL-60 and Jurkat cells in G0/G1 phase increased and that in S phase decreased after being treated with atorvastatin for 24 hours compared with that in control group, suggesting that the atorvastatin can retard the three cells in the G0/G1 phase. The study find that the basal expressions of TLR4, MYD88 and NF-?B gene in K562, HL-60 and Jurkat cells are obviously down-regulated in a dose-dependent manner after being treated with atorvastatin with different concentrations. This down-regulation action of atorvastatin to the expression of the TLR4, MYD88 and NF-?B gene becomes more obvious with the increase of the drug level. In addition, the PI3K, AKT and their phosphorylation levels in the above cells down-regulate obviously in a dose-dependent manner after being treated with atorvastatin. This down-regulation action of atorvastatin to the PI3K, AKT and their phosphorylation levels become more obvious with the increase of the drug level. Conclusions: Atorvastatin can inhibit proliferation and induce apoptosis in leukemia cells, which may be associated with the regulation of atorvastatin to the TLR4/MYD88/PI3K/AKT/NF-?B signaling pathway. äStudy on the function and mechanism of atorvastatin in regulating leuk(epmc).pdf DeepDyve Pubget Overpricing