Fig. 4
dBET1 protects against inflammatory and oxidative damage in the ischemic cortex. A Effect of dBET1 on neuroinflammation following tMCAO was examined by measuring the mRNA levels of pro-inflammatory cytokines and chemokines IL-1β, IL-6, TNF-α, Ccl2, Cxcl1, and Cxcl10 in peri-infarct regions of cortex at 48 h after tMCAO. Compared to sham controls, stroke evoked a prominent increase in the above markers, which were significantly suppressed by dBET1 treatment. n = 5 per sham group, n = 6 stroke veh group, n = 7 stroke dBET1 group. *P < 0.05, **P < 0.01, ***P < 0.001. B Representative western immunoblots showed the expression levels of 4-HNE-modified proteins and NADPH oxidase isoform NOX2 (GP91phox), two oxidative stress markers, and SOD2 and GPX1, two antioxidant proteins, in the ischemic cortex at 48 h after tMCAO and sham controls. β-actin was used as a loading control. C Quantitative analysis in B showed that stroke led to a significant increase in 4 HNE and GP91phox and a decline in SOD2 and GPX1, which were reduced by dBET1. n = 5 per sham group, n = 6 per stroke group. *P < 0.05, **P < 0.01, ***P < 0.001