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A Mouse Model of Orthopedic Surgery to Study Postoperative Cognitive Dysfunction and Tissue Regeneration
Published on: February 27, 2018
Electroacupuncture Attenuates Neuroinflammation and Postoperative Cognitive Dysfunction in Aged Rats by Suppressing
Baobao Ma1,2,3, Shiwen Fan1,4, Jiaojiao Deng1
1Department of Anesthesiology, First Affiliated Hospital, Shihezi University, Shihezi 832003, China.
Electroacupuncture (EA) alleviates postoperative cognitive dysfunction (POCD) in aged rats by inhibiting the cGAS-STING pathway and reducing neuroinflammation. This study suggests EA as a promising non-pharmacological strategy for managing POCD.
Area of Science:
- Neuroscience
- Immunology
- Integrative and Complementary Medicine
Background:
- Postoperative cognitive dysfunction (POCD) is a significant complication in elderly patients, often linked to surgery-induced neuroinflammation.
- The cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) pathway is a key regulator of innate immunity and has been implicated in neuroinflammation.
Purpose of the Study:
- To investigate if electroacupuncture (EA) can improve POCD in aged rats by modulating the hippocampal cGAS-STING pathway.
- To assess the impact of EA on neuroinflammation and cognitive function in a rat model of POCD.
Main Methods:
- An aged rat model of POCD was established using sevoflurane anesthesia and splenectomy.
- Cognitive function was assessed using the Morris water maze test.
- Hippocampal expression and localization of cGAS-STING pathway components (cGAS, STING, IRF3, NF-κB, IL-1β) were analyzed via Western blot and immunofluorescence.
Main Results:
- POCD rats exhibited significant spatial memory impairments and increased hippocampal expression of cGAS, STING, NF-κB, IRF3, and IL-1β.
- cGAS and STING proteins were found to be co-localized with neurons in the hippocampus.
- EA treatment partially reversed these cognitive deficits and molecular changes, an effect mirrored by cGAS inhibition.
Conclusions:
- Electroacupuncture effectively alleviates POCD in aged rats.
- The mechanism involves the inhibition of hippocampal cGAS-STING pathway activation and subsequent reduction in neuroinflammation.
- EA presents a potential non-pharmacological therapeutic strategy for managing POCD.
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