Miao Liu1, Rong Tang1, Yi Jiang1. 1. Department of Paediatrics, Renmin Hospital, Wuhan University Wuhan 430060, Hubei Province, P.R. China.
Abstract
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-κB 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 μmol/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-κB 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-κB 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-κB 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-κB signaling pathway.
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-κB 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 μmol/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-κB 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-κB 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-κB 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-κB signaling pathway.
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