Figure 1

3-MA treatment inhibits ischemia-induced activation of cathepsin B or cathepsin L–tBid–mitochondrial apoptotic signaling pathway in the ischemic cortex. 3-MA (150, 300 and 600 nmol) or vehicle was administrated icv 10 min after ischemia induced by pMCAO. (a) Brain slice stained with 2, 3, 5- triphenyltetrazolium chloride (TTC). The region within the blue line indicates the part of the ischemic brain cortex collected as samples for western blotting analysis. (b-g) Representative western blotting images of the protein levels of active cathepsin B (b) at 6 h or cathepsin L (c) at 3 h, tBid (d), mitochondrial (e) and cytoplastic Cyt-c (f) and active caspase-3 (g) at 24 h after ischemia. (h-m) Columns represent quantitative analysis of immunoblots in (b-g), respectively (means±S.D., n=3). Cyt-c oxidase IV (COX IV), which is located in the inner mitochondrial membrane acts as a mitochondrial marker. β-Actin or HSP-60 was used as a loading control. ##P<0.01 versus Sham group; *P<0.05, **P<0.01 versus ischemic control group (IC)