The Role of Nrf2 in D-Galactose-Induced Cardiac Aging in Mice: Involvement of Oxidative Stress

  • Gerontology. 2021;67(1):91-100. doi: 10.1159/000510470.
Xilan Yang  1 ,  Jian Jia  1 ,  Ling Ding  1 ,  Zhen Yu  1 ,  Chen Qu  2
Affiliations
  • 1. The Second Affiliated Hospital of Nanjing Medical University, Nanjing, China.
  • 2. The Second Affiliated Hospital of Nanjing Medical University, Nanjing, China, [email protected].
PMID: 33271531 DOI: 10.1159/000510470
Abstract

Introduction: Cardiac aging is the major risk factor for advanced heart disease, which is the leading cause of death in developed countries, accounting for >30% of deaths worldwide.

Objective: To discover the detailed mechanism of cardiac aging and develop an effective therapeutic candidate drug to treat or delay cardiac aging.

Methods: We used D-galactose to induce cardiac aging in Nrf2+/+ and Nrf2-/- mice, and then treated these mice with vehicle or the Nrf2 activator, CDDO-imidazolide (CDDO-Im).

Results and conclusions: D-galactose injection significantly induced cardiac aging, cell Apoptosis, and oxidative stress in Nrf2+/+ mice, all of which were further exacerbated in Nrf2-/- mice. CDDO-Im treatment can effectively weaken oxidative stress and enhance the activities of antioxidant Enzymes, but CDDO-Im lost its antioxidative effect in the Nrf2-/- mice. Nrf2 activator CDDO-Im could therefore effectively protect against D-galactose-induced cardiac aging by inhibiting oxidative stress, suggesting that CDDO-Im might be a potential and promising therapeutic candidate drug to treat cardiac aging.

Keywords
CDDO-imidazolide; Cardiac aging; D-galactose; Nrf2; Oxidative stress.
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