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Fig. 8 | Journal of Neuroinflammation

Fig. 8

From: The potential neuroprotective role of a histone deacetylase inhibitor, sodium butyrate, after neonatal hypoxia-ischemia

Fig. 8

Effects of SB on the expression of COX-2, NfκB, p53, and HSP70 in the brain after neonatal HI. Seven-day-old rats (PND7) were subjected to hypoxia-ischemia followed by 24 and 48 h and 6 days of recovery. SB or vehicle was administered directly after the onset of HI and for 2 or 5 consecutive days (determined by the experimental paradigm). Figure shows representative immunoblots of COX-2 (a), NfκB (c), p53 (e), and HSP-70 (g) protein in brain hemispheres, analyzed in four experimental groups: vehicle control (C), SB-treated control (C + SB), vehicle-treated hypoxia-ischemia (HI), and SB-treated hypoxia-ischemia (HI + SB). The intensity of each band obtained by respective Western blotting was quantified by LKB Ultrascan XL software and normalized in relation to β-actin. Bar graphs (b, d, f, h) represent statistical analysis of densitometric data (OD units) from indicated experimental groups. Note the decrease of HI-induced elevation of COX-2 immunoreactivity after SB treatment at 6 days of recovery. The administration of SB also resulted in an increased expression of HSP70 protein at the same time point. The values represent means ± SD from five animals. The one-way ANOVA and Bonferroni test: *p < 0.05, **p < 0.01. C control, ipsi ipsilateral, contra contralateral

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