Fig. 7

Overexpression of CHMP2A alleviates neuroinflammation and improves neurologic outcomes and neuropathological damage after CA. a, b Representative Western blot analyses of AIM2, IL-1β, and IL-18 protein levels in the motor cortex after exposure to CA-ROSC. c, d Representative immunofluorescence images and quantification of IL-1β (red) and DAPI (blue) double staining in the motor cortex of the sham, CA, CA+LV-Vector, and CA+LV-CHMP2A groups. Scale bar, 50 μm. e, f Representative immunofluorescence images and quantification of IL-18 (red) and DAPI (blue) double staining in the motor cortex of the sham, CA, CA+LV-Vector, and CA+LV-CHMP2A groups. Scale bar, 50 μm. g Scatter plots showing the difference in the distribution of NDSs (0 = brain death; 80 = normal) between the vector and CHMP2A groups. The data are presented as medians and interpercentile ranges (n = 6–7), two-factor (group × time) repeated-measures ANOVA. *P < 0.05, ***P < 0.001, and ****P < 0.0001. h Balance beam test scores of rats from each group. i Overexpression of CHMP2A decreased the number of Nissl-stained degenerative neurons in the motor cortex 72 h after CA-ROSC. Scale bar, 50 μm. The small red squares in the coronal section of the brain indicate the area observed. The red arrowheads indicate degenerative neurons with condensed staining and shrunken cytoplasm. j Quantification of Nissl-stained neuronal survival in the motor cortex. The data are expressed as means ± SEM (n = 4–6), one-way ANOVA. **P < 0.01, ***P < 0.001, and ****P < 0.0001 vs. sham