Research Paper Volume 13, Issue 3 pp 3405—3427

PTP1B inhibitor alleviates deleterious microglial activation and neuronal injury after ischemic stroke by modulating the ER stress-autophagy axis via PERK signaling in microglia


Figure 1. Upregulation of PTP1B protein expression after cerebral ischemia/reperfusion (IR) injury. (A) PTP1B protein was detected by western blot in the rat ipsilateral cortex 12, 24, and 72 h after cerebral IR injury, and was normalized to GAPDH. Quantitative results of relative band density are presented as the mean ± SEM (n = 4 per group). (B) Double immunofluorescence staining to detect cell type distribution of PTP1B in microglia (Iba-1), astrocytes (GFAP), and neurons (NeuN) in ipsilateral cerebral cortex 24 h after cerebral IR injury. Scale bar = 50 μm. (C) Quantitative analysis of the percentage of PTP1B-positive cell in microglia, astrocytes, and neurons after cerebral IR injury are presented as the mean ± SEM (n = 6 per group). (D) Flow cytometry to determine the cell type ratio of PTP1B in ipsilateral cortical microglia (Iba-1), astrocytes (GFAP), and neurons (NeuN) 24 h after cerebral IR injury. (E) Quantitative analysis of (D). The results are presented as the mean ± SEM (n = 5 per group). *p < 0.05; **p < 0.01; ***p < 0.001 compared with the sham group; IR = ischemia/reperfusion.