Spatiotemporal Characterization of GSTO1 Inhibition in Postoperative Cognitive Dysfunction: Roles of Hippocampal Oxidative Stress and Neuroinflammation in Aged Mice
Abstract
Abstract Objective This preliminary study evaluated the time-dependent effects of hippocampal glutathione S-transferase omega 1 (GSTO1) inhibition on postoperative cognitive function, oxidative stress, and neuroinflammation in aged mice. Methods Seventy-two aged C57BL/6 mice were randomized into four groups (n=18/group): Surgery+C1-27, Surgery+Vehicle, C1-27 only, and Control. Following Morris water maze pre-training, the respective interventions were performed. Spatial memory, hippocampal GSTO1 expression level, oxidative stress markers (ROS, MDA, GSH/GSSG ratio), pro-inflammatory cytokines (TNF-α, IL-1β, IL-6), and amyloid precursor protein (APP) deposition were dynamically evaluated at 6 h, 3 d, and 7 d post-modeling. Results Pharmacological GSTO1 inhibition combined with surgical trauma induced an acute decline in hippocampal GSTO1 expression at 6 h, along with a marked reduction of the GSH/GSSG ratio ( P P Conclusion Surgical trauma and pharmacological GSTO1 inhibition drive a multi-phase pathological cascade characterized by acute impairment of hippocampal antioxidant defense, progressive neuroinflammation, and structural APP accumulation, which ultimately lead to exacerbated spatial memory deficits. These descriptive findings suggest that GSTO1-regulated microenvironmental homeostasis is critically involved in perioperative cognitive decline, establishing a foundation for future genetic causal validation.
How strong is the evidence?
Evidence Hub reads this as a preprint, done in animal, not in people. Its evidence level is 5 of 5 (Very low · case / narrative / animal / in vitro / in silico). Case reports, narrative reviews, and animal, cell or computer-model studies give the weakest evidence for human health. Reported size: 18 participants or records.
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