Protective effects of EGCG on acrolein-induced Caenorhabditis elegans and its mechanism of life extension.

ABSTRACT

In this study, it was found that epigallocatechin-3-gallate (EGCG) could extend the lifespan of Caenorhabditis elegans (C. elegans) induced by 100 µM acrolein (ACR) at all test concentrations (300, 400, 500, 600, and 700 µM). Notably, 500 µM EGCG exhibited the most significant mean lifespan extension, increasing it by approximately 32.5%. Furthermore, 500 µM EGCG effectively reduced elevated levels of reactive oxygen species (ROS) and lipofuscin production caused by acrolein. It also bolstered the activity of antioxidant enzymes and mitigated malondialdehyde (MDA) levels compared to the ACR-only group. These effects appeared independent of dietary restrictions. Additionally, qPCR results revealed different changes in the transcription levels of 11 genes associated with antioxidative and anti-aging functions following EGCG treatment. At the expression level, GST-4GFP, SOD-3GFP and HSP-16.2GFP exhibited an initial increase with ACR treatment followed by a decrease with EGCG treatment, while the expression pattern of these three GFPs remained consistent with the enzyme activity and transcription regulation level. EGCG treatment also reduced the nuclear localization of SKN-1 and DAF-16 in the MAPK and IIS pathways that were enhanced by ACR. Moreover, the longevity-promoting effects of EGCG were diminished or absent in 13 longevity gene-deletion mutants. In conclusion, EGCG demonstrates protective effects on ACR-induced C. elegans, with the IIS and MAPK pathways playing a critical role in enhancing resilience to ACR.