Neuroinflammation and neuronal autophagic death were suppressed via Rosiglitazone treatment: New evidence on neuroprotection in a rat model of global cerebral ischemia

Ischemic stroke is one of the leading causes of mortality and disability with documented high incidence and relapse rate. Accumulating evidence indicates that autophagy participated in neuronal cell death and functional loss induced following ischemia/reperfusion (I/R) injury. The peroxisome proliferating activating receptor-γ (PPAR-γ) agonist, Rosiglitazone (RSG), is known for its anti-inflammatory actions. Previous studies have demonstrated that RSG can exert neuroprotection in animal models of both chronic brain injuries and acute brain insults.
Source: Journal of the Neurological Sciences - Category: Neurology Authors: Source Type: research