Affiliations: [a] School of Basic Medical Sciences, Hangzhou Normal University, China
| [b] Laboratory of Aging and Cancer Biology of Zhejiang Province, Hangzhou Normal University, China
| [c] School of Food Science and Biotechnology, Zhejiang Gongshang University, China
| [d] Weifang Elbe Health Food Co., LTD, China
Correspondence:
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Correspondence to: Dr. Huanhuan Wang, School of Basic Medical Sciences, Hangzhou Normal University, Yuhangtang Rd. 2318#, Hangzhou, 311121, China. E-mail: [email protected] and Dr. Xuan Zhu, School of Food Science and Biotechnology, Zhejiang Gongshang University, Xuezheng Str. 18#, Hangzhou, 310018, China. E-mail: [email protected].
Abstract: Background:Fine particulate matter (particulate matter 2.5, PM2.5) is considered one of the harmful factors to neuronal functions. Apoptosis is one of the mechanisms of neuronal injury induced by PM2.5. Methylcobalamine (MeCbl) has been shown to have anti-apoptotic and neuroprotective effects. Objective:The current work tried to explore the neuroprotective effects and mechanisms that MeCbl protects mice against cognitive impairment and neuronal apoptosis induced by chronic real-time PM2.5 exposure. Methods:Twenty-four 6-week-old male C57BL/6 mice were exposed to ambient PM2.5 and fed with MeCbl for 6 months. Morris water maze was used to evaluate the changes of spatial learning and memory ability in mice. PC12 cells and primary hippocampal neurons were applied as the in vitro model. Cell viability, cellular reactive oxygen species (ROS) and the expressions of apoptosis-related proteins were examined. And cells were stained with JC-1 and mitochondrial membrane potential was evaluated. Results:In C57BL/6 mice, MeCbl supplementation alleviated cognitive impairment and apoptosis-related protein expression induced by PM2.5 exposure. In in vitro cell model, MeCbl supplementation could effectively rescue the downregulation of cell viability induced by PM2.5, and inhibited the increased levels of ROS, cellular apoptosis, and the expressions of apoptosis related proteins related to PM2.5 treatment, which may be associated with modulation of mitochondrial function. Conclusion:MeCbl treatment alleviated cognitive impairment and neuronal apoptosis induced by PM2.5 both in vivo and in vitro. The mechanism for the neuroprotective effects of MeCbl may at least be partially dependent on the regulation of mitochondrial apoptosis.
