Effect of Chloroquine on Doxorubicin-induced Apoptosis in A549 Cells
Effect of Chloroquine on Doxorubicin-induced Apoptosis in A549 Cells
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DOI：
10.21873/anticanres.15899
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发表时间：
2022-07
影响因子：
2
通讯作者：
Keisuke Sato;Natsuki Ota;Shoya Endo;A. Nakata;Hiroshi Yamashita;R. Tatsunami
中科院分区：
文献类型：
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作者：
Keisuke Sato;Natsuki Ota;Shoya Endo;A. Nakata;Hiroshi Yamashita;R. Tatsunami
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。材料和方法：用阿霉素、氯喹或两者处理 A549 细胞。然后，测量细胞毒性。还对半胱天冬酶和丝裂原激活蛋白激酶的表达水平进行了定量。此外，还测量了阿霉素衍生的活性氧的水平。结果：氯喹增强阿霉素诱导的细胞凋亡和氧化应激，并抑制阿霉素诱导的细胞外信号调节激酶激活。结论：氯喹增强阿霉素诱导的和氧化应激介导的细胞凋亡。该机制可能涉及细胞外信号调节激酶的去磷酸化。
Background/Aim: We investigated the effects of chloroquine, an autophagy inhibitor, on doxorubicin-induced apoptosis in A549 cells. Materials and Methods: 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. Results: Chloroquine enhanced doxorubicin-induced apoptosis and oxidative stress and suppressed the doxorubicin-induced extracellular-signal-regulated kinase activation. Conclusion: Chloroquine enhances doxorubicin-induced and oxidative stress-mediated apoptosis. This mechanism may involve the dephosphorylation of extracellular-signal-regulated kinases.