Butylene fipronil induces apoptosis in PC12 murine nervous cells via activation of p16-CDK4/6-cyclin D1 and mitochondrial apoptotic pathway
文献类型： 外文期刊
作者： Zhong, Shi 1 ; Zhu, Jianxun 1 ; Li, Yougui 1 ; Wang, Xinquan 2 ; Yu, Jiaqi 3 ; Ji, Dongfeng 1 ; Wu, Chongming 3 ;
作者机构： 1.Zhejiang Acad Agr Sci, Sericultural Res Inst, Hangzhou 310021, Zhejiang, Peoples R China
2.Zhejiang Acad Agr Sci, Key Lab Detect & Control Pesticide Residues, Hangzhou, Zhejiang, Peoples R China
3.Chinese Acad Med Sci, Pharmacol & Toxicol Res Ctr, Inst Med Plant Dev, Beijing 100193, Peoples R China
4.Peking Union Med Coll, Beijing 100193, Peoples R China
关键词： apoptosis; butylene fipronil; G0/G1-phase arrest; PC12 cells; reactive oxygen species
期刊名称：JOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY （ 影响因子：3.642； 五年影响因子：3.222 ）
ISSN： 1095-6670
年卷期： 2019 年 33 卷 3 期
页码：
收录情况： SCI
摘要： Butylene fipronil (BFPN) is a phenylpyrazole insecticide, acting at the gamma-aminobutyric acid (GABA) receptor. Here, we show that BFPN inducedcytotoxicity in PC12 murinenervous cells, which lacks GABA receptor. Treatment with BFPN for 48 hours significantly enhanced G0/G1 arrest and induced apoptosis. BFPN decreased the expression of cyclin-dependent kinase (CDK4 and CDK6) and increased P16 and cyclin D1. Simultaneously, Bcl-2 protein was declined while Bax and cytochrome c were significantly enhanced in BFPN-treated groups. The apoptotic enzymes caspase-8, -9, and -3 were also activated by BFPN. Furthermore, treatment with BFPN significantly stimulated reactive oxygen species (ROS) generation, and pretreatment with antioxidant diphenyleneiodonium, substantially reduced cell death. Overall, these results suggest that BFPN is effective to induce G0/G1-phase arrest and apoptosis in PC12 murine nervous cell. Stimulating ROS generation and activation of P16-CDK4/6-cyclin D1 and mitochondrial apoptotic pathway may participate in the cytotoxicity of BFPN.
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