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Published on: June 10, 2013
miR-423-3p alleviates sevoflurane-induced learning and memory dysfunction and nerve damage via negative regulation of
Liquan Qiu1, Licai Zhang1, Bin Fan1
1Department of Anesthesiology, Zigong Fourth People's Hospital, Zigong 643000, China.
Background:
Sevoflurane anesthesia, while widely used, is associated with several side effects including the potential for nerve damage. MicroRNAs are disrupted in patients with sevoflurane anesthesia, including miR-423-3p. However, the association between miR-423-3p and neurological damage remains to be elucidated.
Aim:
To investigate the effect of miR-423-3p on the rats after sevoflurane anesthesia and related molecular mechanisms.
Methods:
RT-qPCR was utilized to quantify the levels of miR-423-3p, GPX4 and oxidative stress indicators in rat hippocampus. Cognitive function was assessed through the Morris water maze and novel object recognition tests. ELISA was applied to detect the levels of inflammatory factors.
Results:
In the Sev group, miR-423-3p expression was significantly elevated, while GPX4 expression was markedly reduced. Down-regulated miR-423-3p negatively regulated GPX4 to shorten escape latency while increasing crossing times of the platform, time spend in the target quadrant, relative occupancy of exploring new objects and time to explore new objects. Furthermore, down-regulated miR-423-3p reduced ROS and MDA levels and increased GSH levels in nerve-injured rats, which could be reversed by inhibited GPX4. miR-423-3p inhibition reduced the levels of NLRP3, Caspase-1, IL-8, and IL-1β, which could be rescued by inhibition of GPX4.
Conclusion:
Down-regulation of miR-423-3p attenuated cognitive deficits in nerve-injured rats. Moreover, repressed miR-423-3p mitigated oxidative stress and inflammation by negatively regulating GPX4.
Insights
Down-regulating miR-423-3p in rats reduced cognitive deficits after sevoflurane anesthesia. This repression mitigated oxidative stress and inflammation by negatively regulating GPX4, offering a potential therapeutic target.
Area of Science:
- Neuroscience
- Molecular Biology
- Anesthesiology
Background:
- Sevoflurane anesthesia can cause nerve damage, with altered microRNA expression, including miR-423-3p.
- The specific role of miR-423-3p in sevoflurane-induced neurological damage is not fully understood.
Purpose of the Study:
- To investigate the impact of miR-423-3p on rats following sevoflurane anesthesia.
- To elucidate the molecular mechanisms underlying miR-423-3p's effect on neurological damage.
Main Methods:
- Quantitative real-time PCR (RT-qPCR) to measure miR-423-3p, GPX4, and oxidative stress markers in the rat hippocampus.
- Behavioral tests (Morris water maze, novel object recognition) to assess cognitive function.
- Enzyme-linked immunosorbent assay (ELISA) to quantify inflammatory factors.
Main Results:
- Sevoflurane anesthesia increased miR-423-3p and decreased GPX4 expression.
- Down-regulated miR-423-3p improved cognitive function and reduced oxidative stress (ROS, MDA) and inflammation (NLRP3, Caspase-1, IL-8, IL-1β) by negatively regulating GPX4.
- GPX4 inhibition reversed the protective effects of miR-423-3p down-regulation.
Conclusions:
- Down-regulation of miR-423-3p attenuates cognitive deficits and nerve injury in rats exposed to sevoflurane.
- Repressed miR-423-3p alleviates oxidative stress and inflammation, primarily through the negative regulation of GPX4.
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