Abstract: Ischemic stroke triggers a complex cascade of events involving inflammation, oxidative stress, and glial cell dysfunction, all of which contribute to neuronal damage and impaired recovery. Glial cells (e.g., astrocytes, microglia, and oligodendrocytes) play key roles in neuroinflammatory responses, making them attractive targets for therapeutic modulation. Cannabidiol, a non-psychoactive phytocannabinoid from Cannabis sativa, exhibits anti-inflammatory, antioxidant, and neuroprotective properties. Preclinical evidence indicates that cannabidiol attenuates glial reactivity, reduces pro-inflammatory signaling, mitigates oxidative stress, and preserves blood–brain and intestinal barrier integrity in stroke models. Moreover, cannabidiol modulates key molecular pathways (e.g., nuclear factor-κB, tumor necrosis factor, and calcium-related signaling), contributing to reduced infarct volume and improved neurological function. Despite these promising effects, clinical translation is hindered by a lack of standardized formulations, dosing regimens, and human trials. This review highlights the impact of cannabidiol on glial cell activity in ischemic stroke, proposing it as a multi-target agent with therapeutic potential in post-stroke recovery and neuroprotection.

Key words: blood–brain barrier, cannabidiol, endocannabinoid system, glial cells, ischemic stroke, neuroinflammation, neuroprotection, oxidative stress