Figure 1: A deficiency in STAT3 activation in GFAP+ NSCs and astrocytes in Trpv1−/− mouse brains upon the peripheral LPS stimulation. | Scientific Reports

Figure 1: A deficiency in STAT3 activation in GFAP+ NSCs and astrocytes in Trpv1−/− mouse brains upon the peripheral LPS stimulation.

From: TRPV1 is crucial for proinflammatory STAT3 signaling and thermoregulation-associated pathways in the brain during inflammation

Figure 1

C57BL/6J mice received an intraperitoneal administration of 50 μg/kg LPS and were sacrificed for STAT3 immunohistochemistry. (a,b) The nuclear translocation of STAT3 was often observed in GFAP+ NSCs in sensory CVOs (OVLT, SFO, and AP) and thermoregulatory hypothalamic subregions (MnPO and POA) in Trpv1+/+ mice 2 hr after the peripheral LPS stimulation (top and middle panels in a), while it was rarely observed in Trpv1−/− mice (b). A three-dimensional image analysis demonstrated the presence of STAT3+ nuclei in GFAP+ NSCs and astrocytes (bottom panels in a). Arrowheads indicate STAT3+ nuclei in GFAP+ cells. Scale bars = 50 (top panels of a,b) and 10 (bottom panels of a) μm. (c) The quantitative analysis showed that the number of STAT3+ GFAP+ cells in Trpv1+/+ mice was significantly increased in sensory CVOs and hypothalamic thermoregulatory brain subregions after the intraperitoneal administration of 50 μg/kg LPS, but was not in Trpv1−/− mice. Sol, solitary nucleus; 3V, 3rd ventricle. Data (n = 4) were expressed as the mean (±s.e.m.). *P < 0.05, ***P < 0.001 vs the vehicle in Trpv1+/+ mice and #P < 0.05, ###P < 0.001 between Trpv1+/+ and Trpv1−/− mice by ANOVA with Turkey’s post hoc tests.

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