Inhibition of advanced glycation endproducts formation by lotus seedpod oligomeric procyanidins through RAGE-MAPK signaling and NF-κB activation in high-AGEs-diet mice

This study investigated the modulatory effects of lotus seedpod oligomeric procyanidins (LSOPC) on the advanced glycation endproducts (AGEs)-induced liver injury via advanced glycation end-product receptors (RAGE)-mitogen-activated protein kinases (MAPK)-nuclear factor-kappa B (NF-kappa B) signaling pathways in a mice model. To examine the antioxidation properties of LSOPC, a model of high-AGEs-diet were established using Sprague Dawley (SD) male mice fed with a normal AIN-93G diet, a high AGEs diet (H), or H plus 0.5 or 0.2% (w/w) LSOPC for 12 weeks. Our results showed that LSOPC inhibited the AGEs formation and alleviated AGEsinduced liver injury by suppressing the nuclear translocation of NF-kappa B and activation of the MAPK signaling pathway. Additionally, LSOPC inhibited the genes expression of tumor necrosis factor-alpha (TNF-alpha) and interleukin 6 (IL-6). Taken together, LSOPC treatment potentially inhibited the AGEs formation and modulated liver injury with long-term dietary AGEs by suppressing RAGE-MAPK-NF-kappa B pathways.

Automated summary

The study demonstrated that LSOPC inhibited AGEs formation, alleviated AGEs-induced liver injury by suppressing NF-kappa B nuclear translocation and MAPK signaling pathway activation. Additionally, LSOPC also inhibited the expression of TNF-alpha and IL-6. In conclusion, LSOPC treatment potentially modulated liver injury caused by long-term dietary AGEs by suppressing the RAGE-MAPK-NF-kappa B pathways.