Department of Pharmacy, Hokkaido University of Science, Sapporo, Japan.
Department of Pharmacy, Hokkaido University of Science, Sapporo, Japan
Anticancer Res. 2022 Aug;42(8):4025-4035. doi: 10.21873/anticanres.15899.
BACKGROUND/AIM: We investigated the effects of chloroquine, an autophagy inhibitor, on doxorubicin-induced apoptosis in A549 cells.
A549 cells were treated with doxorubicin, chloroquine, or both. Then, cytotoxicity was measured. The expression levels of caspases and mitogen-activated protein kinases were also quantified. In addition, the levels of doxorubicin-derived reactive oxygen species were measured.
Chloroquine enhanced doxorubicin-induced apoptosis and oxidative stress and suppressed the doxorubicin-induced extracellular-signal-regulated kinase activation.
Chloroquine enhances doxorubicin-induced and oxidative stress-mediated apoptosis. This mechanism may involve the dephosphorylation of extracellular-signal-regulated kinases.
背景/目的:我们研究了自噬抑制剂氯喹对阿霉素诱导的 A549 细胞凋亡的影响。
用阿霉素、氯喹或两者处理 A549 细胞,然后测量细胞毒性。还定量了半胱天冬酶和丝裂原活化蛋白激酶的表达水平。此外,还测量了阿霉素衍生的活性氧的水平。
氯喹增强了阿霉素诱导的细胞凋亡和氧化应激,并抑制了阿霉素诱导的细胞外信号调节激酶的激活。
氯喹增强了阿霉素诱导的氧化应激介导的细胞凋亡。这种机制可能涉及细胞外信号调节激酶的去磷酸化。