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Peroxisome proliferator-activated receptor-gamma agonists induce neuroprotection following transient focal ischemia in normotensive, normoglycemic as well as hypertensive and type-2 diabetic rodents

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dc.creator Vemuganti, Raghu
dc.creator Bowen, Kellie K.
dc.creator Satriotomo, Irawan
dc.creator Liang, Jin
dc.creator Feinstein, Douglas L.
dc.creator Kapadia, Ramya
dc.creator Tureyen, Kudret
dc.date 2007-04-01T00:00:00Z
dc.date.accessioned 2021-12-03T11:30:08Z
dc.date.available 2021-12-03T11:30:08Z
dc.identifier 6c4ceb1d-b70e-403e-ad6f-bb6333e9845b
dc.identifier 10.1111/j.1471-4159.2006.04376.x
dc.identifier https://avesis.sdu.edu.tr/publication/details/6c4ceb1d-b70e-403e-ad6f-bb6333e9845b/oai
dc.identifier.uri http://acikerisim.sdu.edu.tr/xmlui/handle/123456789/92410
dc.description Thiazolidinediones (TZDs) are synthetic agonists of the ligand-activated transcription factor peroxisome proliferator-activated receptor-gamma (PPAR gamma). TZDs are known to curtail inflammation associated with peripheral organ ischemia. As inflammation precipitates the neuronal death after stroke, we tested the efficacy of TZDs in preventing brain damage following transient middle cerebral artery occlusion (MCAO) in adult rodents. As hypertension and diabetes complicate the stroke outcome, we also evaluated the efficacy of TZDs in hypertensive rats and type-2 diabetic mice subjected to transient MCAO. Pre-treatment as well as post-treatment with TZDs rosiglitazone and pioglitazone significantly decreased the infarct volume and neurological deficits in normotensive, normoglycemic, hypertensive and hyperglycemic rodents. Rosiglitazone neuroprotection was not enhanced by retinoic acid x receptor agonist 9-cis-retinoic acid, but was prevented by PPAR gamma antagonist GW9662. Rosiglitazone significantly decreased the post-ischemic intercellular adhesion molecule-1 expression and extravasation of macrophages and neutrophils into brain. Rosiglitazone treatment curtailed the post-ischemic expression of the pro-inflammatory genes interleukin-1 beta, interleukin-6, macrophage inflammatory protein-1 alpha, monocyte chemoattractant protein-1, cyclooxygenase-2, inducible nitric oxide synthase, early growth response-1, CCAAT/enhancer binding protein-beta and nuclear factor-kappa B, and increased the expression of the anti-oxidant enzymes catalase and copper/zinc-superoxide dismutase. Rosiglitazone also increased the expression of the anti-inflammatory gene suppressor of cytokine signaling-3 and prevented the phosphorylation of the transcription factor signal transducer and activator of transcription-3 after focal ischemia. Thus, PPAR gamma activation with TZDs might be a potent therapeutic option for preventing inflammation and neuronal damage after stroke with promise in diabetic and hypertensive subjects.
dc.language eng
dc.rights info:eu-repo/semantics/closedAccess
dc.title Peroxisome proliferator-activated receptor-gamma agonists induce neuroprotection following transient focal ischemia in normotensive, normoglycemic as well as hypertensive and type-2 diabetic rodents
dc.type info:eu-repo/semantics/article


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