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Dexmedetomidine Ameliorates Postoperative Cognitive Dysfunction in Aged Mice.
Xiaolan Xie1, Zhiwen Shen2,3, Chuwen Hu2,3
1Department of Anesthesiology, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, 510120, China.
Neurochemical Research
|June 23, 2021
Summary
Dexmedetomidine (Dex) alleviates surgery-induced cognitive impairment by reducing neuroinflammation and oxidative stress. This study shows Dex protects against postoperative cognitive dysfunction (POCD) in aged mice.
Area of Science:
- Neuroscience
- Pharmacology
- Gerontology
Background:
- Neuroinflammation and oxidative stress are key factors in postoperative cognitive dysfunction (POCD) and neurodegenerative diseases.
- Dexmedetomidine (Dex) is known for its anti-inflammatory and antioxidant effects, but its role in mitigating surgery-induced cognitive decline is not fully understood.
Purpose of the Study:
- To investigate the neuroprotective mechanisms of Dexmedetomidine (Dex) against surgery-induced cognitive impairment in aged mice.
- To explore whether Dexmedetomidine (Dex) can ameliorate cognitive deficits associated with oxidative stress and inflammation post-surgery.
Main Methods:
- An aged mouse model of abdominal exploratory laparotomy was used to induce cognitive dysfunction.
- Mice were pretreated with Dexmedetomidine (20 µg/kg) before surgery.
- Cognitive function was assessed using the Open Field Test (OFT) and Morris Water Maze (MWM).
- Hippocampal tissues were analyzed for inflammatory markers, oxidative stress indicators, apoptosis-related proteins, and microglial activation.
Main Results:
- Surgery induced cognitive impairment in mice, which was significantly alleviated by Dexmedetomidine (Dex) pretreatment.
- Dex reduced pro-inflammatory cytokines and microglial activation in the hippocampus.
- Dex decreased malondialdehyde (MDA) levels and increased superoxide dismutase (SOD) activity.
- Dex modulated CDK5 activity, increased Brain-Derived Neurotrophic Factor (BDNF) expression, and reduced the Bax/Bcl-2 ratio, suppressing apoptosis.
Conclusions:
- Dexmedetomidine (Dex) exerts neuroprotective effects against surgery-induced cognitive impairment in aged mice.
- These protective effects are mediated through anti-inflammatory and antioxidant actions.
- Dex also suppresses the mitochondrial permeability transition pore and apoptosis-related pathways, offering a potential therapeutic strategy for postoperative cognitive dysfunction (POCD).
