Abstract Title:

Neuroinflammatory response to experimental stroke is inhibited by eriodictyol.

Abstract Source:

Behav Brain Res. 2016 10 1 ;312:321-32. Epub 2016 Jun 25. PMID: 27353856

Abstract Author(s):

Emerson de Oliveira Ferreira, Mara Yone Soares Dias Fernandes, Neila Maria Rocha de Lima, Kelly Rose Tavares Neves, Marta Regina Santos do Carmo, Francisco Arnaldo Viana Lima, Analu Aragão Fonteles, Ana Paula Fontenele Menezes, Geanne Matos de Andrade

Article Affiliation:

Emerson de Oliveira Ferreira


BACKGROUND: Cerebral ischemia is a common disease and one of the most common causes of death and disability worldwide. The lack of glucose and oxygen in neuronal tissue leads to a series of inflammatory events, culminating in neuronal death. Eriodictyol is a flavonoid isolated from the Chinese herb Dracocephalum rupestre that has been proven to have anti-inflammatory properties.

HYPOTHESIS/PURPOSE: Thus, the present study was designed to explore whether eriodictyol has neuroprotective effects against the neuronal damage, motor and memory deficits induced by permanent middle cerebral artery occlusion (pMCAO) in mice.

STUDY DESIGN: Animals were orally treated with eriodictyol (1, 2 and 4mg/kg) or vehicle (saline) 30min before pMCAO, 2h after, and then once daily for the following five days.

METHODS: The parameters studied were neuronal viability, brain infarcted area; sensorimotor deficits; exploratory activity; working and aversive memory; myeloperoxidase (MPO) activity; TNFα, iNOS and GFAP immunoreactivity.

RESULTS: The treatment with eriodictyol prevented neuronal death, reduced infarct area and improved neurological and memory deficits induced by brain ischemia. The increase of MPO activity and TNF-α, iNOS and GFAP expression were also reduced by eriodictyol treatment.

CONCLUSION: These findings demonstrate that eriodictyol exhibit promising neuroprotection effects against the permanent focal ischemia cerebral injury in the mice experimental model and the underlying mechanisms might be mediated through inhibition of neuroinflammation.

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