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. Author manuscript; available in PMC: 2012 Feb 1.
Published in final edited form as: Arterioscler Thromb Vasc Biol. 2010 Nov 11;31(2):289–296. doi: 10.1161/ATVBAHA.110.217901

Figure 2. PKC inhibition attenuates calpain activity in the hyperglycemic, insulin-deficient microcirculation.

Figure 2

Following superfusion of the rat mesentery with the fluorogenic calpain substrate t-BOC-Leu-Met-CMAC, active calpains in the venular endothelium were visualized by fluorescent intravital microscopy and measured by densitometry. Control post-capillary venules (V) had a very low basal level of calpain activity indicated by a low level of fluorescent staining (Panel A). Calpain activity was markedly increased in the post-capillary venular endothelium of STZ-diabetic rats, as demonstrated by intense fluorescent staining (Panel B, white arrows). The PKC inhibitor BIM-I reduced fluorescent staining for calpain activity in the STZ-diabetic microcirculation (Panel C). The calpain inhibitor PD150606 also attenuated fluorescent staining for calpain activity. White line in Panel A represents 10 µm scale. Yellow circle in panel B depicts a representative region of interest (ROI) used for densitometry. The bar graph shows densitometry quantification of calpain activity in all experimental groups of rats. Bars represent mean ± SEM, and numbers at the base of the bars represent the number of rats studied in each group.