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. Author manuscript; available in PMC: 2013 Jul 4.
Published in final edited form as: Basic Res Cardiol. 1998 Oct;93(5):325–338. doi: 10.1007/s003950050101

Fig. 9.

Fig. 9

Measurements of NF-κB DNA binding activity (electrophoretic mobility shift assay) in the ischemic/reperfused left ventricular region of conscious rabbits undergoing ischemic PC. All values are expressed as a percentage of the values in the control group (group I), which did not undergo ischemia. A marked rise in the DNA binding activity was noted 30 min after the ischemic PC protocol (six 4-min coronary occlusion/4-min reperfusion cycles) (group II). This increase in DNA binding activity was completely abrogated when DDTC (an inhibitor of NF-κB, group III), MPG (a scavenger of OH and ONOO, group IV), L-NA (a NOS inhibitor, group V), chelerythrine (an inhibitor of PKC, group VI), or LD-A (an inhibitor of tyrosine kinases, group VII) were administered before the ischemic PC protocol. Interestingly, when DETA/NO was administered in the absence of PC ischemia (group VIII), there was a marked increase in NF- κ B DNA binding activity similar to that in preconditioned rabbit hearts (group II). *P< 0.05 vs. group I; §P< 0.05 vs. group II (n = 4 in all groups).