0000000000199855

AUTHOR

Phuriphong Songarj

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The antioxidative, non-psychoactive tricyclic phenothiazine reduces brain damage after experimental traumatic brain injury in mice.

2014

Abstract Oxidative stress due to free radical formation is an important mechanism of secondary brain damage following traumatic brain injury (TBI). Phenothiazine has been found to be a strong antioxidant in eukaryotic cells in vitro and in invertebrates in vivo. The present study was designed to determine the neuroprotective potency of unsubstituted phenothiazine in a paradigm of acute brain injury. Thirty minutes after pneumatic, controlled cortical impact (CCI) injury, C57BI6 mice were randomly assigned to “low dose” (3 mg/kg, LD) or “high dose” (30 mg/kg, HD) s.c. phenothiazine or vehicle treatment. Brain lesion, neurofunctional impairment, body weight, and markers of cerebral inflammati…

MaleTraumatic brain injuryGene ExpressionInflammationCell CountBrain damagePharmacologymedicine.disease_causeNeuroprotectionAntioxidantsRandom AllocationIn vivoPhenothiazinesMedicineAnimalschemistry.chemical_classificationInflammationDose-Response Relationship Drugbusiness.industryGeneral NeuroscienceCalcium-Binding ProteinsMicrofilament ProteinsBrainmedicine.diseaseMice Inbred C57BLchemistryAnesthesiaBrain InjuriesTumor necrosis factor alphamedicine.symptombusinessNeurogliaOxidative stressTricyclicNeuroscience letters
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