Beijing Institute of Dental Research, Beijing Stomatological Hospital and School of Stomatology, Capital Medical University , Beijing, China.
Suzhou Stomatological Hospital , Suzhou, China.
Biotech Histochem. 2020 Nov;95(8):626-633. doi: 10.1080/10520295.2020.1749304. Epub 2020 May 4.
Local action of nicotine on oral mucosa contributes to the pathogenesis of precancerous and cancerous lesions. Nicotine participation in the mechanism of apoptosis in normal mucosa has not been established. Peroxiredoxin 1 (Prx1) is a cellular antioxidant that participates in regulating apoptosis. We investigated expression of Prx1 and proteins in apoptosis-related downstream signaling by mitogen-activated protein kinases (MAPKs) in nicotine-treated tongue tissues of wild-type and Prx1 knockout (Prx1) mice; we also investigated these processes in mouse embryonic fibroblast (MEF) cells in vitro. Nicotine increased the expression of Prx1 mRNA in tongue tissues in vivo. The rate of apoptosis was similar among the nicotine-treated mice, nicotine-treated + Prx1 mice and untreated controls. The expression of p-JNK was greater in Prx1 mice compared to control mice. In MEF cells, nicotine increased the expression of Prx1 and inhibited apoptosis and expression of p-p38 and p-JNK. Prx1 knockdown animals exhibited increased apoptotic rate and expression of p-p38 and p-JNK in MEFs. Nicotine-regulated apoptosis might occur via a Prx1-dependent pathway.
尼古丁对口腔黏膜的局部作用导致癌前病变和癌症的发生。尼古丁在正常黏膜细胞凋亡机制中的作用尚未确定。过氧化物酶 1（Prx1）是一种细胞抗氧化剂，参与调节细胞凋亡。我们研究了在野生型和 Prx1 敲除（Prx1）小鼠的尼古丁处理舌组织中，丝裂原活化蛋白激酶（MAPKs）下游信号转导相关蛋白的凋亡和 Prx1 的表达；我们还在体外研究了这些过程在小鼠胚胎成纤维细胞（MEF）中的作用。尼古丁增加了体内舌组织中 Prx1 mRNA 的表达。在尼古丁处理的小鼠、尼古丁处理+Prx1 小鼠和未处理的对照组中，细胞凋亡率相似。与对照组相比，Prx1 小鼠中 p-JNK 的表达更高。在 MEF 细胞中，尼古丁增加了 Prx1 的表达，抑制了细胞凋亡和 p-p38 和 p-JNK 的表达。Prx1 敲低的动物在 MEFs 中表现出更高的凋亡率和 p-p38 和 p-JNK 的表达。尼古丁调节的细胞凋亡可能通过 Prx1 依赖的途径发生。
