Abstract��OBJECTIVE To investigate the effects and mechanism of itraconazole (Itra) on proliferation in lung cancer A549 cell line.METHODS A549 cells were treated with indiacted dose of Itra for 24, 48 and 96h. The cell survival rate was detected by MTT and the semi-inhibitory concentration (IC50) was calculated. The cells were divided into four groups including control group, Itra group, compound C (Comp C) +Itra group, 4-PBA+ Itra group. The apoptosis was detected by AnnexinV/PI. Western blot(WB) was used to detect the expression of CHOP, GRP78, PERK, Bcl-2, Bax, AMPK, phosphorylated-AMPK(p-AMPK). RESULTS The survival rate of A549 cells was inhibited by Itra. The IC50 at 24, 48, and 96h were 62.89, 28.34 and 11.64 ��mol��L-1 respectively. Compared with control group, the cell survival rate decreased, the apoptosis rate increased obviously in Itra group. Compared with group Itra, the cell survival rate decreased, the apoptosis rate increased in Comp C +Itra group and 4-PBA+ Itra group(P��0.05). Compared with control group, the expression of CHOP, GRP78, PERK and p-AMPK increased in Itra group(P��0.05). The expression of CHOP, GRP78, PERK and p-AMPK were lower in Comp C +Itra group and 4-PBA+ Itra group than that in control group(P��0.05). CONCLUTION Itra induces endoplasmic reticulum stress related apoptosis via activating AMPK signaling.
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