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041) and a trend toward increased bleeding (HT) (Figure 3). This was manifested in a significantly worse functional outcome in terms of neurologic score (P = 0.028) and paw grasp (P = 0.022) in the candesartan-treated groups (Figure 3). There were no significant differences in thiram edema formation in any of the treatment groups. Figure 3 Effects of candesartan alone and in combination with FeTPPS and GM6001 on infarct size (a, d), edema (b, e), and hemoglobin content (c, f) at 24h after MCAO. Infarct size and Hb content were significantly reduced in all three treatment groups ... 4. Discussion The neuroprotective effects of the angiotensin receptor antagonists are well documented in experimental cerebral ischemia ALK inhibitor [13], but their robust vascular protective effects [11, 17, 31] appear to be incompatible with the demonstrated ability to increase MMP-2 and MMP-9 activity [17]. The experiments reported here represent attempts to determine the mechanism of the early vascular protective effects of candesartan so that other interventions can be developed that do not have the attendant blood pressure lowering properties. Reperfusion after ischemia increases levels of reactive oxygen species, including superoxide radical [32] and nitric oxide (NO) [33]. Oxidative radicals trigger activation of MMPs after ischemic stroke [34]. Superoxide reacts with NO to form peroxynitrite. Oxygen-glucose deprivation or INCB28060 order reperfusion after cerebral ischemia increases peroxynitrite in cerebral endothelial cells and neurons [35, 36]. Peroxynitrite is more permeable through the lipid membrane than superoxide [37] and is more toxic [38]. In vitro, peroxynitrite strongly activates MMPs including MMP-9 and MMP-2 [4, 5]. After ischemia reperfusion, peroxynitrite formation on microvessels leads to MMP-9 activation and neurovascular damage (hemorrhage and edema) by disrupting microvascular integrity [2]. Moreover, administration of FeTPPS decreases MMP activation and neurovascular injury through decompositing peroxynitrite levels after cerebral ischemia [9]. In the present study, we test whether administration of a peroxynitrite decomposition catalyst alone and in combination with candesartan after ischemic stroke decreases neurovascular injury. We observed that candesartan mimics the peroxynitrite scavenger in reducing nitrotyrosine. The utility of broad spectrum MMP inhibitors, like GM6001, for experimental work and therapeutic use has been severely limited by their water insolubility. The need to dissolve the agents in DMSO, as we have done in the experiments reported here, introduced unintended consequences of the vehicle itself. DMSO is a nonspecific free radical scavenger that is known to be neuroprotective [39], so any investigation involving its use as a solvent requires a DSMO control group as we have done.