Aceglutamide

Aceglutamide (α-N-Acetyl-L-glutamine; N2-Acetylglutamine) is a neuroprotectant that can penetrate the blood-brain barrier. Aceglutamide can enhance the antioxidant systems of glutathione (GSH), thioredoxin (Trx) and Nrf2. Aceglutamide also inhibits ASK1 and TRAF1, activates the Akt/Bcl-2 anti-apoptotic pathway, enhances the activity of antioxidant enzymes and reduces oxidative damage. Aceglutamide can improve neurological deficits after cerebral ischemia, reduce infarct volume, and inhibit neuronal apoptosis, especially substantia nigra dopaminergic neurons. Aceglutamide can reduce cerebral ischemia/reperfusion injury, improve motor dysfunction, and is used in ischemic stroke-related research^[1][2]. In Vitro:Aceglutamide (1-10 μM; 24 h) improves the cell viability of H₂O₂-induced PC12 cells, reduces the levels of reactive oxygen species (ROS) and nitric oxide (NO), upregulates glutathione (GSH) content and activates the Nrf2/Trx antioxidant system^[1].
Aceglutamide (10 μM; 24 h) inhibits apoptosis in hypoxia/reoxygenation-injured PC12 cells and primary midbrain neurons, improves mitochondrial membrane potential (MMP), downregulates the pro-apoptotic factor TRAF1 and upregulates the Akt/Bcl-2/Bax signaling pathway^[2]. In Vivo:Aceglutamide (50, 150, 300 mg/kg; intraperitoneal injection; once daily; for 14 consecutive days) improves neurological deficits and reduces cerebral infarct volume in a dose-dependent manner in the cerebral ischemia/reperfusion (MCAO) model in male Sprague-Dawley rats, and exerted protective effects by inhibiting the apoptosis of substantia nigra dopaminergic neurons, upregulating the Akt/Bcl-2 pathway, and downregulating TRAF1 protein expression^[1][2].