BackgroundIschemic stroke is a leading cause of death and disability worldwide and is frequently accompanied by brain–gut axis disturbances, including intestinal barrier dysfunction, gut microbiota dysbiosis, and immune–inflammatory imbalance. Although electroacupuncture (EA) has demonstrated neuroprotective effects in experimental stroke, its effects on brain–gut axis-related outcomes have not been systematically evaluated.ObjectiveTo evaluate the effects of EA on neurological outcomes and brain–gut axis-related changes in animal models of ischemic stroke.MethodsThis systematic review and meta-analysis was conducted in accordance with the PRISMA 2020 statement and registered in PROSPERO (CRD420261354722). Nine databases were searched from inception to 1 May 2026. Controlled animal studies comparing EA with non-EA controls in ischemic stroke models were included. Random-effects meta-analyses were performed using Hedges’ g standardized mean differences (SMDs) with 95% confidence intervals (CIs). Risk of bias was assessed using the SYRCLE tool, and the certainty of evidence was evaluated using an adapted GRADE framework for preclinical animal studies.ResultsThirteen reports representing 12 independent studies were included. EA was associated with improved neurological function (11 studies; SMD = −2.49, 95% CI: −3.50 to −1.47; I2 = 60.5%) and reduced infarct volume (9 studies; SMD = −3.08, 95% CI: −4.22 to −1.95; I2 = 56.2%). EA was also associated with increased ZO-1, occludin, and intestinal IL-10 levels and reduced D-lactate, lipopolysaccharide, intestinal IL-1β, and intestinal TNF-α levels. Qualitative synthesis suggested EA-associated changes in gut microbial diversity and taxonomic composition, although their functional significance remains uncertain. The certainty of evidence ranged from moderate to very low, and several brain–gut axis-related outcomes were supported by only a small number of studies.ConclusionEA-related neuroprotection in ischemic stroke may be partially associated with modulation of brain–gut axis-related processes; however, the available evidence does not establish these processes as the primary mediator. Further rigorously designed preclinical studies are needed to strengthen causal inference and facilitate clinical translation.Systematic review registrationhttps://www.crd.york.ac.uk/PROSPERO/view/CRD420261354722, Identifier: CRD420261354722.