Effect of dihydroferulic acid obtained from fermented rice bran extract on neuroprotection and behavioral recovery in an ischemic rat model

Abstract This study aimed to evaluate whether dihydroferulic acid (dFA) promoted the viability of H2O2-treated PC12 cells and functional recovery from ischemic injury. The animals were divided into four groups for the study: (1) the vehicle treated (saline, 1 mL/kg), (2) dFA 5 mg/kg treated, (3) dFA...

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Main Authors: Sang Hyun LEE, Dana YEO, Jeong Hwa HONG
Format: Article
Language:English
Published: Sociedade Brasileira de Ciência e Tecnologia de Alimentos
Series:Food Science and Technology
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Online Access:http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0101-20612020005012206&lng=en&tlng=en
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Summary:Abstract This study aimed to evaluate whether dihydroferulic acid (dFA) promoted the viability of H2O2-treated PC12 cells and functional recovery from ischemic injury. The animals were divided into four groups for the study: (1) the vehicle treated (saline, 1 mL/kg), (2) dFA 5 mg/kg treated, (3) dFA10 mg/kg treated, and (4) dFA 20 mg/kg treated groups. Neurological deficit was evaluated using the modified neurological severity score. Real-time polymerase chain reaction analyses were performed with the protein disulphide isomerase (PDI), nuclear factor-E2-related factor 2 (Nrf2), nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) genes. Immunohistochemical analysis was performed with the Iba-1 and MFG-E8 genes. dFA treatment improved the reduced viability of PC12 cells induced by H2O2 in a dose-dependent manner. Only 50 μM of dFA significantly enhanced the transcription levels of antioxidant genes and neurotrophic factors compared to the vehicle group. In vivo dFA administration exerted a neuroprotective effect by reducing the infarct volume and enhancing behavioral function following cerebral ischemia. dFA treatment protected neuronal cells from ischemic injury and increased the transcription levels of anti-oxidant genes (PDI and Nrf2) and neurotrophic factors (BDNF and NGF). dFA treatment decreased the expression of Iba-1 and MFG-E8 genes, which signal neural cell death.
ISSN:0101-2061
1678-457X