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过氧化物酶 V 的敲低增加了非热等离子体处理的培养基对 A549 细胞的细胞毒性。

Knockdown of Peroxiredoxin V increased the cytotoxicity of non-thermal plasma-treated culture medium to A549 cells.

机构信息

Stem Cell and Regenerative Biology Laboratory, College of Life Science and Biotechnology, Heilongjiang Bayi Agricultural University, Daqing 163319, Heilongjiang, China.

Yabian Academy of Agricultural Science, Longjing 1334000, Jilin, China.

出版信息

Aging (Albany NY). 2022 May 11;14(9):4000-4013. doi: 10.18632/aging.204063.

DOI:10.18632/aging.204063
PMID:35546738
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9134956/
Abstract

Administration of non-thermal plasma therapy via the use of plasma-activated medium (PAM) might be a novel strategy for cancer treatment, as it induces apoptosis by increasing reactive oxygen species (ROS) levels. Peroxiredoxin V (PRDX5) scavenges ROS and reactive nitrogen species and is known to regulate several physiological and pathological reactions. However, its role in lung cancer cells exposed to PAM is unknown. Here, we investigated the effect of in PAM-treated A549 lung cancer cells and determined the mechanism underlying its cytotoxicity. Cell culture medium was treated with low temperature plasma at 16.4 kV for 0, 60, 120, or 180 s to develop PAM. was knocked down in A549 cells via transfection with short hairpin RNA targeting . Colony formation and wound healing assays, flow cytometry, fluorescence microscopy, and western blotting were performed to detect the effect of knockdown on PAM-treated A549 cells. PAM showed higher cytotoxicity in lung cancer cells than in control cells, downregulated the mitogen-activated protein kinase signaling pathway, and induced apoptosis. knockdown significantly inhibited cell colony formation and migration, increased ROS accumulation, and reduced mitochondrial membrane potential in lung cancer cells. Hence, knockdown combined with PAM treatment represents an effective option for lung cancer treatment.

摘要

通过使用等离子体激活介质（PAM）进行非热等离子体治疗可能是一种治疗癌症的新策略，因为它通过增加活性氧（ROS）水平诱导细胞凋亡。过氧化物酶 V（PRDX5）清除 ROS 和活性氮物种，并已知调节几种生理和病理反应。然而，其在暴露于 PAM 的肺癌细胞中的作用尚不清楚。在这里，我们研究了在 PAM 处理的 A549 肺癌细胞中 的作用，并确定了其细胞毒性的机制。将细胞培养基在 16.4 kV 下用低温等离子体处理 0、60、120 或 180 s 以开发 PAM。通过靶向 的短发夹 RNA 转染将 敲低 A549 细胞。进行集落形成和伤口愈合测定、流式细胞术、荧光显微镜和 Western blot 以检测 敲低对 PAM 处理的 A549 细胞的影响。与对照细胞相比，PAM 在肺癌细胞中表现出更高的细胞毒性，下调丝裂原活化蛋白激酶信号通路，并诱导细胞凋亡。 敲低显着抑制肺癌细胞的集落形成和迁移，增加 ROS 积累，并降低线粒体膜电位。因此，与 PAM 治疗联合使用 敲低代表了治疗肺癌的有效选择。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ec7/9134956/63658acff5e1/aging-14-204063-g008.jpg
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