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. 2021 Jan 20;13(3):3405–3427. doi: 10.18632/aging.202272

Figure 2.

Figure 2

PTP1B inhibitor treatment attenuated microglial activation and promoted M2 microglial polarization after ischemic injury. (A–C) IL-1β, IL-6, and TNF-α mRNA levels after the OGD/R insult were tested by real-time PCR in rat primary microglia. Fold-changes were normalized to β-actin and quantitative results are presented as the mean ± SEM (n = 5 per group). (D) Outline of in vivo experiment to detect the effect of intracerebroventricular administration of PTP1B inhibitor after cerebral IR injury. (E) Immunohistology to detect CD11b/c cell in the ipsilateral cerebral cortex, and quantitative analysis of CD11b/c-positive cell number are presented as the mean ± SEM (n = 5 per group). Scale bar = 50 μm. (F, G) Double immunofluorescence to detect CD16/32(+) Iba-1(+) cell in ipsilateral cerebral cortex 72 h after IR injury, and quantitative analysis of CD16/32(+) Iba-1(+) cell density (presented as the mean ± SEM, n = 6 per group). Scale bar = 50 μm. (H, I) Double immunofluorescence to detect CD206(+) Iba-1(+) cells in the ipsilateral cerebral cortex 72 h after IR injury, and quantitative analysis of CD206(+) Iba-1(+) cell density (presented as the mean ± SEM, n = 6 per group). Scale bar = 50 μm. (J) Quantitative analysis of the ratio of Iba1(+)/CD206(+) microglia to Iba-1(+)/CD16/32(+) microglia; the results are presented as the mean ± SEM. *p < 0.05; **p < 0.01; ***p < 0.001 compared with vehicle group; sc = sc-222227, a PTP1B inhibitor; i.c.v. = intracerebroventricular injection; IR = ischemia/reperfusion; R = reperfusion; OGD/R = oxygen glucose deprivation/reoxygenation.