Abstract Title:

Therapeutic effects of chrysin in a rat model of traumatic brain injury: A behavioral, biochemical, and histological study.

Abstract Source:

Life Sci. 2019 Jul 1 ;228:285-294. Epub 2019 May 4. PMID: 31063733

Abstract Author(s):

Masome Rashno, Alireza Sarkaki, Yaghoob Farbood, Mohammad Rashno, Layasadat Khorsandi, Mohammad Kazem Gharib Naseri, Mahin Dianat

Article Affiliation:

Masome Rashno


AIMS: Oxidative stress and apoptosis have major roles in the progression of traumatic brain injury (TBI)-associated motor and cognitive deficits. The present study was aimed to elucidate the putative effects of chrysin, a natural flavonoid compound, against TBI-induced motor and cognitive dysfunctions and possible involved mechanisms.

MAIN METHODS: Chrysin (25, 50 or 100 mg/kg) was orally administered to rats starting immediately following TBI induction by Marmarou's weight-drop technique and continuously for 3 or 14 days. Neurological functions, motor coordination, learning and memory performances, histological changes, cell apoptosis, expression of pro- and anti-apoptotic proteins, and oxidative status were assayed at scheduled time points after experimental TBI.

KEY FINDINGS: The results indicated that treatment with chrysin improved learning and memory disabilities in passive avoidance task, and ameliorated motor coordination impairment in rotarod test after TBI. These beneficial effects were accompanied by increased the concentrations of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione (GSH), decreased malondialdehyde (MDA) content, prevented neuronal loss, diminished apoptotic index, elevated the expression of anti-apoptotic Bcl-2 protein, and reduced the expression of pro-apoptotic Bax protein in the cerebral cortex and hippocampus tissues.

SIGNIFICANCE: Our findings suggest that both anti-oxidative and anti-apoptotic properties of chrysin (especially in the dose of 100 mg/kg) are possible mechanisms that improve cognitive/motor deficits and prevent neuronal cell death after TBI.

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