机构：[1]Faculty of Life Science and Technology, Kunming University of Science and Technology, Kunming, China[2]Research Institute of Nutrition and Food Science, Kunming Medical University, Kunming, China[3]Department of Gastroenterology, Yunnan First People’s Hospital, Kunming, China内科片消化内科云南省第一人民医院[4]Yunnan Yunce Quality Testing Co., Ltd, Kunming, China[5]Yunnan Key Laboratory of Nutrition and Food Safety, Kunming Medical University, Kunming, China
Purpose: The aim of this study was to explore the mechanism of neurological changes underlying the toxicity of nicotine. Materials and methods: Rat pheochromocytoma 12 (PC12) cells and human neuroglia (HM) cells were used. The ROS levels of the cells were detected by the FACScan. Autophagy flux was monitored by a tandem monomeric RFP-GFP-tagged LC3 lentivirus. The autophagic proteins LC3, SQSTM1/p62 and Beclin1 were detected by western blot assay. In order to evaluate the effects of nicotine and melatonin on the morphological changes of neurons, primary cortical neurons were obtained and immunocytochemistry of TUBB3 tubulin were conducted. Results: Nicotine increased the levels of reactive oxygen species (ROS) in PC12 and HM cells in a concentration-dependent manner. Microscopy showed increased autophagic flux in nicotine-treated PC12 cells. Subsequent western blotting results showed that nicotine induced increase in the levels of LC3B-II and Beclin1, and decreased SQSTM1/p62 in a concentration-dependent manner. Finally, nicotine treatment reduced the length of TUBB3-positive axons and dendrites. Melatonin, a mitochondrially targeted antioxidant, reduced the ROS level, and blocked autophagy activation and the morphologic structural changes induced by nicotine. Conclusions: Our results suggested that the role of nicotine in neuronal toxicity maybe through the induction of ROS and the subsequent activation of autophagy. These effects could be restored by melatonin.
基金：
This work was supported by the National Natural Science
Foundation of China under Grant [number 81560101 and
81601767]; the Yunnan Applied Basic Research Project under
Grant [number 2016FB124]; and Key Project of Yunnan
Education Department [number 2015Z073].
第一作者机构：[1]Faculty of Life Science and Technology, Kunming University of Science and Technology, Kunming, China
共同第一作者：
通讯作者：
通讯机构：[2]Research Institute of Nutrition and Food Science, Kunming Medical University, Kunming, China[5]Yunnan Key Laboratory of Nutrition and Food Safety, Kunming Medical University, Kunming, China[*1]Research Institute of Nutrition and Food Science, Kunming Medical University, 1168 West Chunrong Road, Yuhua Avenue, Chenggong District, Kunming 650500, Yunnan, P.R. China.
推荐引用方式(GB/T 7714)：
Feng Yue,Xu Fang,Wang Song-Mei,et al.Melatonin attenuates nicotine-induced autophagy and neurological changes by decreasing the production of reactive oxygen species[J].INTERNATIONAL JOURNAL OF NEUROSCIENCE.2020,130(4):391-397.doi:10.1080/00207454.2019.1692833.
APA：
Feng, Yue,Xu, Fang,Wang, Song-Mei,Wu, Shao-Xiong,Zhang, Xue-Hui...&Feng, Yue-Mei.(2020).Melatonin attenuates nicotine-induced autophagy and neurological changes by decreasing the production of reactive oxygen species.INTERNATIONAL JOURNAL OF NEUROSCIENCE,130,(4)
MLA：
Feng, Yue,et al."Melatonin attenuates nicotine-induced autophagy and neurological changes by decreasing the production of reactive oxygen species".INTERNATIONAL JOURNAL OF NEUROSCIENCE 130..4(2020):391-397
