Skip to main content
Fig. 7 | Journal of Neuroinflammation

Fig. 7

From: A novel role for protein tyrosine phosphatase 1B as a positive regulator of neuroinflammation

Fig. 7

PTP1B inhibitor suppressed microglial activation in a mouse neuroinflammation model. a C57BL/6 mice were injected i.c.v. with vehicle (saline containing 0.5 % DMSO and 5 % propylene glycol) or PTP1B inhibitor (diluted in saline containing 5 % propylene glycol). At 30 min after the injection of PTP1B inhibitor, mice were injected i.p. with LPS (5 mg/kg). The mice were anesthetized and transcardially perfused with ice-cold saline 48 h after the LPS injection. The expression of PTP1B in the brain 48 h after the LPS injection was measured by RT-PCR. GAPDH was used for the loading control. b The brains were removed and the sections were stained with Iba-1 (a marker for microglia). Iba-1-positive cells were observed in the cortex, hippocampus (hippo), and thalamus region of mouse brains. Scale bar, 50 μm. c. The graph shows activated microglial cell number per square millimeter. NS not significant. The expression levels of proinflammatory genes were determined by real-time RT-PCR 48 h after the LPS injection. Levels of TNF-α (d) and IL-1β mRNA (e) were normalized to β-actin levels and expressed as fold increase. *p < 0.05 versus LPS + vehicle-injected animals; analyzed by one-way ANOVA with Tukey’s multiple comparison test. f Phosphorylation of Y527 Src in brain 48 h after LPS i.p. injection with or without PTP1Bi i.c.v. administration. Phospho (Y527)- and total Src protein levels were determined by western blot analysis. β-actin levels were used as loading controls. Lcn2 was used as a neuroinflammatory marker

Back to article page