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Updated: Jan 16, 2026
A Mouse Model of Orthopedic Surgery to Study Postoperative Cognitive Dysfunction and Tissue Regeneration
Published on: February 27, 2018
Increased reactive astrocytes in hippocampal CA1 region mediated by decreased CXCR7 is involved in postoperative
Qiang Liu1, Chen-Rui Zhou2, Hai-Bi Wang2
1Department of Anesthesiology and Perioperative Medicine, Shanghai Key Laboratory of Anesthesiology and Brain Functional Modulation, Clinical Research Center for Anesthesiology and Perioperative Medicine, Translational Research Institute of Brain and Brain-Like Intelligence, Shanghai Fourth People's Hospital, School of Medicine, Tongji University, Shanghai, 200434, China.
Abstract:
Postoperative cognitive dysfunction (POCD) is a prevalent neurological complication that significantly impairs recovery in elderly surgical patients. While astrocyte activation has been implicated in various neurodegenerative disorders, its dynamic changes and precise role in POCD pathogenesis remain poorly understood. In this study, we observed selective activation of astrocytes (but not microglia) in the hippocampal CA1 region of POCD model mice at postoperative day 3, accompanied by marked downregulation of the atypical chemokine receptor CXCR7. Notably, both astrocyte-specific CXCR7 overexpression in the hippocampal CA1 region and systemic administration of the CXCR7 agonist AMD3100 effectively attenuated astrocyte activation, reduced neuroinflammation, and significantly improved synaptic plasticity and cognitive performance in aged surgical mice. Furthermore, chemogenetic inhibition of hippocampal astrocytes during the perioperative period similarly ameliorated neuroinflammatory responses and cognitive deficits. Our findings demonstrate that surgery induces reactive astrogliosis in the hippocampal CA1 region through CXCR7 downregulation, ultimately leading to synaptic dysfunction and cognitive impairment. These results identify CXCR7 as a promising therapeutic target for POCD prevention.
