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. Author manuscript; available in PMC: 2014 Feb 1.
Published in final edited form as: J Neurochem. 2012 Dec 28;124(4):523–535. doi: 10.1111/jnc.12111

Fig.3.

Fig.3

Distribution of C3 was suppressed by PBN in neurons and microglia after tFCI in mice. (a) Positive staining for C3 (red) was highly revealed in the ipsilateral region compared with the sham region after tFCI in the WT mice. PBN-treated brains showed less C3 compared with vehicle-treated brains. Co-staining with neuronal and microglial cell-type markers (green) distinctly revealed C3 in neurons and microglia after cerebral I/R injury. Neurons and microglia were also highly activated after tFCI in the vehicle group compared with the PBN group. C3 co-localization with neurons or microglia after tFCI was significantly reduced by PBN treatment. Yellow (white arrows) indicates colocalization of anti-C3 with anti-NeuN or anti-Iba-1 (***p<0.001, n=20, compared to vehicle-treatment group). Scale bar, 40 μm. (b) The C3 protein level in the nucleus was significantly suppressed by PBN compared with the vehicle after tFCI. C3a and C5a protein levels were markedly decreased by PBN compared with the vehicle. TFIID was used as an internal control for nucleus (*p<0.05 and ***p<0.001, n=6, comparison between vehicle- and PBN-treated mice at the same time points). TFIID indicates transcription factor II D.