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Phenothiazine Inhibits Neuroinflammation and Inflammasome Activation Independent of Hypothermia After Ischemic Stroke
In conclusion, C + P treatment conferred neuroprotection in stroke by suppressing neuroinflammation and NLRP3 inflammasome activation. The present study suggests that JAK2/STAT3/p38/HIF-1α/FoxO1 are vital regulators and potential targets for efficacious therapy following ischemic stroke.
Source: Molecular Neurobiology - August 29, 2021 Category: Neurology Source Type: research

Phosphoenolpyruvate Carboxykinase (PCK) in the Brain Gluconeogenic Pathway Contributes to Oxidative and Lactic Injury After Stroke
AbstractTo demonstrate the role of the rate-limiting and ATP-dependent gluconeogenic enzyme phosphoenolpyruvate carboxykinase (PCK) in oxidative and lactic stress and the effect of phenothiazine on PCK after stroke, a total of 168 adult male Sprague Dawley rats (3  months old, 280–300 g) underwent 2-h intraluminal middle cerebral artery occlusion (MCAO) and reperfusion for 6, 24, 48 h, or 7 days. Phenothiazine (chlorpromazine and promethazine (C+P)) (8 mg/kg) and 3-mercaptopicolinic acid (3-MPA, a PCK inhibitor, 100 μM) were administered at reperfusi on onset. The effects of phosphoenolpyruvate, 3-MPA, or PCK knoc...
Source: Molecular Neurobiology - January 8, 2021 Category: Neurology Source Type: research

Erratum to: Neuroprotection by Chlorpromazine and Promethazine in Severe Transient and Permanent Ischemic Stroke
Source: Molecular Neurobiology - November 14, 2017 Category: Neurology Source Type: research