5 results about "Nrf2 activators" patented technology

The invention relates to application of odd-carbon fatty acid as an Nrf2 activator, in particular to application of the odd-carbon fatty acid or a composition containing the odd-carbon fatty acid to preparation of a medicament for treating and / or preventing Nrf2 pathway mediated diseases or symptoms. The invention also relates to an application of odd-carbon fatty acids or a composition thereof in preparation of an Nrf2 agonist and an application of an Nrf2 pathway agonist in preparation of a composition for improving physical conditions of pregnant and / or post-parturition mammals and newborn mammals.

The present invention provides: an Nrf2 activator; and a pharmaceutical composition for preventing or treating diseases related to activation of Nrf2, comprising the Nrf2 activator. Accordingly, it is possible to effectively prevent or treat oxidative stress- or mitochondrial dysfunction-related neurological diseases or oxidative stress-mediated skin diseases.

The application discloses a dihydropyrimidine[4,5-d]pyrimidine-2(H)-ketone Nrf2 activator and a preparation method and application thereof. The compound has the following structural general formula: experiments prove that the compound can effectively activate the Nrf2 signal pathway to produce an antioxidative stress effect, thereby protecting nerve cells, and can be used for preventing and / or treating neurodegenerative diseases.

Cerebral small vessel disease (SVD) is a leading cause of stroke and a major contributor to cognitive decline and dementia in the population. Evidences indicate that blood brain barrier dysfunction may play a significant role in VD pathogenesis. Recently, an inverse association of TRIM47 expression in brain and vascular tissues with extensive-SVD severity was reported in a human genome wide association study combined with summary-based Mendelian randomization studies and profiling of human loss-of-function allele carriers. Now, the inventors demonstrate TRIM47 is a key regulator of actin cytoskeleton organization through KEAP1 / NRF2 signalling pathway and might be protective from oxidative stress in brain EC. In particular, the in vitro TRIM47 knockdown decreases directed EC migration and delays EC adhesion process with loss of actin cortical reorganization and focal adhesion contacts. Furthermore, RNA sequencing and BioID results indicate that TRIM47 knockdown in brain EC, represses the expression of genes associated with cytoskeleton and NRF2 antioxidant pathway through a potential interaction with KEAP1. Accordingly, the present invention relates to the use of Nrf2 activators for the treatment of SVD.