P-Glycoprotein Exacerbates Brain Injury Following Experimental Cerebral Ischemia by Promoting Proinflammatory Microglia Activation

Figure 2

P-glycoprotein regulates inflammatory response and microglial polarization in experimental ischemic stroke. Mice were intracerebroventricularly injected with P-glycoprotein (P-gp) siRNA or negative control (NC) siRNA (1.5 μL/10 g body weight), P-gp p-AAV or NC p-AAV (2.5 μL/10 g body weight), 48 hr or 7 days prior to MCAO/R surgery. Twenty-four hours after the surgery, brains were harvested for RT-PCR and ELISA assays. (a, b) mRNA expression levels of IL-12, IL-6, IL-4, YM-1, CD16, iNOS, CD206, and Arg-1 measured via RT-PCR assay as fold changes relative to sham treatment (n = 4). (c, d) Contents of IL-12, IL-6, IL-4, YM-1, CD16, iNOS, CD206, and Arg-1 determined by ELISA assay (n = 6). (e) Coronal brain diagrams showing locations of regions for molecular analysis in infarct cortex. One-way ANOVA followed by the post hoc least significant difference test or Games Howell test for (a) and (b). Mann–Whitney test for (c) and (d). All data are mean ± SD; , between two groups.

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