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The NRF2 inducer CDDO-2P-Im provokes a reduction in amyloid beta levels in Alzheimer’s disease model mice

ABSTRACT: Alzheimer’s disease (AD) is the most common etiology of dementia. The transcription factor NF-E2-related factor 2 (NRF2) induces the expression of genes encoding phase II detoxification and antioxidant genes. NRF2 is regulated by Kelch-like ECH-associated protein 1 (KEAP1), and the KEAP1-NRF2 system is the key regulatory system involved in cytoprotection. To examine whether pharmacological induction of NRF2 expression alleviates AD phenotypes in vivo, we employed two AD mouse models, i.e., AppNL-G-F/NL-G-F (AppNLGF) and APPV717I::TAUP301L (APP/TAU) mice. As the synthetic oleanane triterpenoid 1-[2-cyano-3,12-dioxooleana-1,9(11-dien-28-oyl)] (CDDO)-4(-pyridin-2-yl)-imidazole (CDDO-2P-Im) exhibits strong NRF2-inducing activity, in this study, we treated AD model mice with CDDO-2P-Im.

ORGANISM(S): Mus musculus

PROVIDER: GSE271154 | GEO | 2024/09/09

REPOSITORIES: GEO

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Pharmacogenomic comparison between D3T- and CDDO-Im in mouse liver tissue

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2018-02-25 | GSE99199 | GEO

Effect of KEAP1 knockout and CDDO-2P-Im Treatment in ARH-77 Cells

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Transcription profiling of mouse Keap1-null (CKO) to investigate genetic and pharmacologic activation of Nrf2 signaling

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Poorly differentiated, human liposarcoma LiSa-2 cell line response to the synthetic triterpenoid CDDO

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