Fig. 2

Schematic illustration of the BBB disruption by IS and the mechanism of DCA protection against ischemic stroke. Increased inflammation and immune response following IS contribute to BBB disruption. Treatment with DCA enhances the expression of anti-inflammatory factors such as IL-10 and CD206, while simultaneously reducing the levels of pro-inflammatory markers including MMP9, TNF-α, IL-6, and iNOS. This suggests that DCA promotes the polarization of small glial cells from the M1 pro-inflammatory phenotype to the M2 anti-inflammatory phenotype. Furthermore, the observed improvement in the expression of BBB-related proteins, such as ZO-1 and occludin, indicates a restoration of the integrity of the BBB