Fig. 5From: Hypochlorous acid derived from microglial myeloperoxidase could mediate high-mobility group box 1 release from neurons to amplify brain damage in cerebral ischemia–reperfusion injuryDynamic changes and localization of MPO expression and HOCl production in ischemic brains during cerebral ischemia–reperfusion injury. Rats were subjected to 2 h of MCAO ischemia alone (I/R-0 h) or 2 h of MCAO ischemia plus 2, 4, 6, 24 h of reperfusion, termed as I/R-2 h, I/R-4 h, 1/R-6 h and I/R-24 h, respectively. MPO expression and HOCl production were detected by western blot analysis and HKOCl-3 staining fluorescence. A MPO expression in brain tissues; B HOCl level in rat brains. Bar = 500 μm. C Quantitative results of HOCl level in rat brains. D Pearson correlation coefficients for correlation between plasma HOCl level and mNSS in rat MCAO I/R injury. N = 16, r = 0.8694, p < 0.001. E Fluorescent imaging of MPO expression in microglia, neuron, and microvascular endothelial cells of the ischemic cortical area by co-stained with Iba-1, NeuN or vWF, respectively. Nucleus was stained with DAPI, bar = 10 μm. F HKOCl-3 staining fluorescent imaging for HOCl production in microglia, neuron, and microvascular endothelial cells co-stained with Iba-1, NeuN or vWF, respectively, nucleus was stained with DAPI, bar = 10 μm. *p < 0.05, **p < 0.01. All data are presented as mean ± SEM. (Statistical methods: A, C one-way ANOVA followed by Tukey’s multiple comparisons test; D Pearson correlation coefficient.)Back to article page