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. 1998 May 1;12(9):1304–1314. doi: 10.1101/gad.12.9.1304

Figure 5.

Figure 5

Figure 5

 Role of caspase-2 in ischemic injury. (A) Brain damage as measured by infarct TTC staining of infarct area 24 hr after permanent focal ischemia in wild-type and caspase-2-deficient mice. Infarct area was determined in each of five coronal sections (2 mm) from anterior (2 mm from anterior pole) to posterior (10 mm from anterior pole) as percent of TTC (○) +/+ (n = 6); (•) −/− (n = 8). (B) Immunoblot of caspase-2 from brain hemisphere on the ischemic side (I) or contralateral side (C) after either transient (3 hr ischemia; 6 hr reperfusion) or permanent (24 hr ischemia) occlusion. Ten micrograms of protein was loaded on the gel per lane. Samples from thymus tissues are shown at left as a comparison for the amount of caspase-2 present in brain and thymus.