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Chalcone-Derived Nrf2 Activator Protects Cognitive Function via Maintaining Neuronal Redox Status.

Yuting Cui¹, Yue Xiong¹, Hua Li¹

¹Center for Mitochondrial Biology and Medicine, The Key Laboratory of Biomedical Information Engineering of Ministry of Education, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an 710049, China.

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|November 27, 2021

Summary

A novel compound, Tak, protects brain cells by activating Nrf2 and the Akt pathway. This reduces oxidative stress and improves cognitive function, showing promise for treating neurodegenerative diseases.

Keywords:

Akt Nrf2 hippocampus mitochondrial function phase II enzymes

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Area of Science:

Neuroscience
Pharmacology
Biochemistry

Background:

NF-E2-related factor 2 (Nrf2) is crucial for neuronal protection.
Chalcone analogs are being investigated for therapeutic potential.

Purpose of the Study:

To evaluate the neuroprotective effects of a novel chalcone analog, Tak.
To investigate the mechanisms underlying Tak's protective actions in vitro and in vivo.

Main Methods:

In vitro studies on cultured neuronal cells.
In vivo studies using mouse models of excitotoxicity, cognitive impairment, and high-fat diet-induced metabolic stress.
Assessment of Nrf2 activation, mitochondrial function, reactive oxygen species levels, apoptosis, and Akt signaling pathway activity.

Main Results:

Tak demonstrated significant hippocampal neuronal protection without toxicity.
Tak increased ATP production, enhanced mitochondrial function, and reduced reactive oxygen species via Nrf2 activation.
Tak treatment ameliorated glutamate-induced excitotoxicity and scopolamine-induced cognitive impairment.
Tak administration improved outcomes in a high-fat diet mouse model by activating Akt-mediated antioxidant pathways.

Conclusions:

Tak protects cognitive function through Akt-mediated Nrf2 activation, maintaining cellular redox balance.
Tak is a potential pharmacological candidate for treating oxidative neuronal diseases.