Bardoxolone methyl prevents high-fat diet-induced alterations in prefrontal cortex signalling molecules involved in recognition memory

Journal article


Camer, Danielle, Yu, Yinghua, Szabo, Alexander, Fernandez, Francesca Elizabeth, Dinh, Chi H. L. and Huang, Xu-Feng. (2015) Bardoxolone methyl prevents high-fat diet-induced alterations in prefrontal cortex signalling molecules involved in recognition memory. Progress in Neuropsychopharmacology and Biological Psychiatry. 59, pp. 68 - 75. https://doi.org/10.1016/j.pnpbp.2015.01.004
AuthorsCamer, Danielle, Yu, Yinghua, Szabo, Alexander, Fernandez, Francesca Elizabeth, Dinh, Chi H. L. and Huang, Xu-Feng
Abstract

High fat (HF) diets are known to induce changes in synaptic plasticity in the forebrain leading to learning and memory impairments. Previous studies of oleanolic acid derivatives have found that these compounds can cross the blood–brain barrier to prevent neuronal cell death. We examined the hypothesis that the oleanolic acid derivative, bardoxolone methyl (BM) would prevent diet-induced cognitive deficits in mice fed a HF diet. C57BL/6J male mice were fed a lab chow (LC) (5% of energy as fat), a HF (40% of energy as fat), or a HF diet supplemented with 10 mg/kg/day BM orally for 21 weeks. Recognition memory was assessed by performing a novel object recognition test on the treated mice. Downstream brain-derived neurotrophic factor (BDNF) signalling molecules were examined in the prefrontal cortex (PFC) and hippocampus of mice via Western blotting and N-methyl-d-aspartate (NMDA) receptor binding. BM treatment prevented HF diet-induced impairment in recognition memory (p < 0.001). In HF diet fed mice, BM administration attenuated alterations in the NMDA receptor binding density in the PFC (p < 0.05), however, no changes were seen in the hippocampus (p > 0.05). In the PFC and hippocampus of the HF diet fed mice, BM administration improved downstream BDNF signalling as indicated by increased protein levels of BDNF, phosphorylated tropomyosin related kinase B (pTrkB) and phosphorylated protein kinase B (pAkt), and increased phosphorylated AMP-activated protein kinase (pAMPK) (p < 0.05). BM administration also prevented the HF diet-induced increase in the protein levels of inflammatory molecules, phosphorylated c-Jun N-terminal kinase (pJNK) in the PFC, and protein tyrosine phosphatase 1B (PTP1B) in both the PFC and hippocampus. In summary, these findings suggest that BM prevents HF diet-induced impairments in recognition memory by improving downstream BDNF signal transduction, increasing pAMPK, and reducing inflammation in the PFC and hippocampus.

Keywordsbardoxolone methyl; hippocampus; 0besity; prefrontal cortex; recognition memory
Year2015
JournalProgress in Neuropsychopharmacology and Biological Psychiatry
Journal citation59, pp. 68 - 75
PublisherElsevier Inc.
ISSN0278-5846
Digital Object Identifier (DOI)https://doi.org/10.1016/j.pnpbp.2015.01.004
Scopus EID2-s2.0-84921969632
Page range68 - 75
Research GroupSchool of Behavioural and Health Sciences
Place of publicationUnited States of America
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