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 7. PTP1B inhibitor treatment reduced neuronal apoptosis, cerebral infarct volume, brain water content, and improved neurologic function after ischemia/reperfusion (IR) injury. (A) Immunofluorescence/TUNEL assays were performed to detect neuronal apoptosis in rat ipsilateral cerebral cortex 24 h after IR injury. Scale bar = 50 μm. (B) The density of NeuN+/TUNEL+ cells was quantified as the mean ± SEM (n = 6 per group). (C) TTC staining were performed to determine infarct volume 24 h after cerebral IR injury. Infarct area was defined as the white area. (D) The infarct volume was quantified as (infarct volume/whole brain volume) × 100% (n = 5 per group). (E) Brain water content. (F) Motor assessment score 3 days after IR injury. (G) Neurologic score 3 days after IR injury. Data for d-g are presented as the mean ± SEM (n = 6 per group). *p < 0.05; **p < 0.01; ***p < 0.001 compared with vehicle group; PTP1Bsc = PTP1B inhibitor sc-222227; IR = ischemia/reperfusion; sc = PTP1B inhibitor sc-222227.