Bcl-2 expression in the ischemic peri-infarct area. Low dose (B) significantly upregulated, whereas high dose (C) significantly suppressed the Bcl-2 expression in the ischemic peri-infarct area of minocycline-treated rats compared to that in the vehicle-treated rats (A). Quantitative analyses of Bcl-2 positive cells are shown in panel D. Data are shown as mean values ± SEM (*p < 0.05). Two representative ischemic striatal peri-infarct areas (+0.2 mm anterior to the bregma), in which Bcl-2 positive cells were counted (data in panel D), are shown in panel E (square boxes). Co-localization of Bcl-2 and MAP2 was found in ischemic striatal peri-infarct area, suggesting anti-apoptotic effects of minocycline via Bcl-2 upregulation in ischemic neurons (F-H). In contrast, GFAP positive astrocytes did not express Bcl-2 (I-K). Scale bar: 25 μm (A-C), 12.5 μm (F-K); asterisks (*): merged cell; green and red immunofluorescent markers correspond to Bcl-2 and MAP2, respectively.
Matsukawa et al. BMC Neuroscience 2009 10:126 doi:10.1186/1471-2202-10-126