Immediate Remote Ischemic Postconditioning Reduces Brain Nitrotyrosine Formation in a Piglet Asphyxia Model

Figure 3

RIPostC-treated animals have increased glial activation. (a–c) IBA1 quantitative thresholding analysis revealed significant increase in microglial IBA1+ staining in the HI + RIPostC group 48 hours after HI. (a) Representative IBA1 staining from the hippocampus at 48 hours after HI in HI alone (upper panel) and HI + RIPostC (lower panel). (b) Mean IBA1 quantitative thresholding analysis across multiple brain regions in HI alone and in RIPostC-treated piglets. (c) Overall IBA1 immunoreactivity was significantly increased in the RIPostC-treated group when compared to HI alone piglets (). (d–f) RIPostC treatment significantly increased GFAP+ astrocytes 48 hours after HI. (d) Representative micrographs of GFAP immunohistochemistry from the hippocampus at 48 hours after HI in HI alone (upper panel) and HI + RIPostC (lower panel). (e) Mean GFAP quantitative thresholding analysis across multiple brain regions in HI alone and in RIPostC-treated piglets. (f) RIPostC treatment resulted in an overall significant increase in GFAP+ astrocyte immunoreactivity 48 hours after HI (). (a, d) Naïve comparative controls are shown on the left panel. Data are expressed as mean ± SEM in ANOVA, per group, and . dCTX1–3 = dorsal cortex 1–3; mCTX = midtemporal cortex; PYR = pyriform cortex; THAL = thalamus; Caudt = caudate; PTMN = putamen; IC = internal capsule; PvWM = periventricular white matter.

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