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Prophylactic Melatonin Treatment Ameliorated Propofol-Induced Cognitive Dysfunction in Aged Rats
Junhua Li1,2,3, Guiyun Wu1,2, Wen Song1,2
1Department of Anesthesiology, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, 510120, China.
Neurotoxicity Research
|November 7, 2020
Summary
Melatonin pretreatment improved propofol-induced cognitive impairment in aged rats. It protected against mitochondrial dysfunction, apoptosis, and synaptic damage, preserving memory function.
Area of Science:
- Neuroscience
- Pharmacology
- Gerontology
Background:
- Melatonin is recognized for its protective effects against cognitive impairments.
- Propofol anesthesia can induce cognitive deficits, particularly in aged individuals.
- Understanding melatonin's neuroprotective mechanisms is crucial for mitigating anesthesia-related cognitive decline.
Purpose of the Study:
- To investigate the precise effects of melatonin pretreatment on cognitive function in aged rats undergoing propofol anesthesia.
- To evaluate melatonin's impact on mitochondrial activity, apoptosis, and synaptic integrity in the hippocampus and prefrontal cortex.
- To elucidate the molecular pathways, including PKA/CREB/BDNF signaling, involved in melatonin's neuroprotective effects.
Main Methods:
- Aged Sprague Dawley rats were randomly assigned to control, propofol-only, or melatonin + propofol groups.
- Cognitive function was assessed using the Barnes maze, open field, and contextual fear conditioning tests.
- Mitochondrial function, apoptosis markers, and PKA/CREB/BDNF signaling were analyzed in hippocampal and prefrontal cortex tissues.
Main Results:
- Melatonin pretreatment significantly improved propofol-induced memory impairment in aged rats.
- Melatonin mitigated mitochondrial dysfunction, reduced apoptotic cell counts in the hippocampus and prefrontal cortex.
- Prophylactic melatonin reversed propofol-induced inactivation of PKA/CREB/BDNF signaling and synaptic dysfunction.
Conclusions:
- Melatonin ameliorates propofol-induced cognitive disorders in aged rats.
- The protective effects are mediated by attenuating mitochondrial dysfunction, apoptosis, and synaptic damage.
- Melatonin's action involves the preservation of the PKA/CREB/BDNF signaling pathway.
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