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Updated: Feb 14, 2026

A Mouse Model of Orthopedic Surgery to Study Postoperative Cognitive Dysfunction and Tissue Regeneration
Published on: February 27, 2018
High-fat diet aggravates postoperative cognitive dysfunction in aged mice
Lan Wei1, Minmin Yao2, Zhimeng Zhao2
1Department of Anesthesia, Zhongshan Hospital Qingpu Branch affiliated to Fudan University, Shanghai, China.
High-fat diets can worsen postoperative cognitive dysfunction (POCD) in aged mice by inhibiting Silent Information Regulator 1 (Sirt1) and promoting neuronal apoptosis. This study investigates the link between diet, Sirt1, and POCD.
Area of Science:
- Neuroscience
- Metabolic Disorders
- Aging Research
Background:
- Postoperative cognitive dysfunction (POCD) and Silent Information Regulator 1 (Sirt1) are key factors in neurodegeneration.
- High-fat diets (HFD) are increasingly linked to neurodegenerative diseases and affect brain Sirt1 and apoptosis.
- The relationship between HFD and POCD remains unclear.
Purpose of the Study:
- To investigate the impact of a high-fat diet on postoperative cognitive dysfunction in aged mice.
- To explore the role of Silent Information Regulator 1 (Sirt1) and apoptosis in diet-induced exacerbation of POCD.
Main Methods:
- Aged C57BL/6 mice were fed either a regular or high-fat diet for 8 weeks.
- Mice underwent surgery under sevoflurane anesthesia to model POCD, or received sham treatment.
- Learning and memory were assessed using the Morris water maze; Sirt1, Bcl-2, Bax, and cleaved caspase-3 levels were measured via western blot.
Main Results:
- High-fat diet impaired learning and memory in control and surgery groups compared to regular diet controls.
- Surgery exacerbated cognitive decline and significantly reduced Sirt1 expression in the hippocampus of high-fat diet mice.
- High-fat diet increased neuronal apoptosis markers (Bax, cleaved caspase-3) and decreased anti-apoptotic marker (Bcl-2), particularly after surgery.
Conclusions:
- High-fat diet exacerbates POCD in aged mice.
- This exacerbation may be mediated by the inhibition of Sirt1 expression and promotion of neuronal apoptosis.
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