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Methylcobalamin Alleviates Neuronal Apoptosis and Cognitive Decline Induced by PM2.5 Exposure in Mice
Xintong Ji1,2, Chenxia Li1,2, Xiaozheng Zhu1
1School of Basic Medical Sciences, Hangzhou Normal University, China.
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.
Insights
Methylcobalamin (MeCbl) protects against cognitive impairment and neuronal apoptosis caused by fine particulate matter (PM2.5) exposure. This neuroprotection involves regulating mitochondrial apoptosis pathways.
Area of Science:
- Neuroscience
- Environmental Health
- Toxicology
Background:
- Fine particulate matter (PM2.5) exposure is a significant risk factor for neuronal dysfunction.
- PM2.5-induced neuronal injury is mediated, in part, by apoptosis.
- Methylcobalamin (MeCbl) exhibits known anti-apoptotic and neuroprotective properties.
Purpose of the Study:
- To investigate the neuroprotective effects of MeCbl against PM2.5-induced cognitive impairment and neuronal apoptosis in mice.
- To elucidate the underlying mechanisms of MeCbl's neuroprotection, focusing on mitochondrial function and apoptosis regulation.
Main Methods:
- In vivo study: C57BL/6 mice exposed to ambient PM2.5 and treated with MeCbl for 6 months, assessed using the Morris water maze.
- In vitro study: PC12 cells and primary hippocampal neurons exposed to PM2.5, with or without MeCbl treatment.
- Evaluations included cell viability, reactive oxygen species (ROS) levels, apoptosis-related protein expression, and mitochondrial membrane potential (JC-1 staining).
Main Results:
- MeCbl supplementation significantly alleviated PM2.5-induced cognitive deficits and apoptosis in mice.
- In vitro, MeCbl rescued cell viability, reduced ROS production, and inhibited apoptosis.
- MeCbl treatment modulated mitochondrial function, suggesting a role in preventing PM2.5-induced mitochondrial dysfunction and apoptosis.
Conclusions:
- MeCbl demonstrates significant neuroprotective effects against PM2.5-induced cognitive impairment and neuronal apoptosis.
- The neuroprotective mechanism of MeCbl is associated with the regulation of mitochondrial apoptosis pathways.
- These findings highlight MeCbl as a potential therapeutic agent for mitigating neurotoxicity from PM2.5 exposure.
