Key Laboratory of Fermentation Engineering (Ministry of Education), Hubei Key Laboratoy of Industrial Microbiology, National "111" Center for Cellular Regulation and Molecular Pharmaceutics, Hubei Research Center of Food Fermentation Engineering and Technology, Hubei University of Technology, Wuhan, Hubei, 430068, China.
Wuhan Institute of Design and Sciences, Wuhan, Hubei, 430205, China.
Food Chem Toxicol. 2021 Oct;156:112481. doi: 10.1016/j.fct.2021.112481. Epub 2021 Aug 8.
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-κB) 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 AGEs-induced liver injury by suppressing the nuclear translocation of NF-κB and activation of the MAPK signaling pathway. Additionally, LSOPC inhibited the genes expression of tumor necrosis factor-α (TNF-α) 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-κB pathways.
本研究通过糖基化终产物受体(RAGE)-丝裂原活化蛋白激酶(MAPK)-核因子-κB(NF-κB)信号通路,探讨了莲子寡聚原花青素(LSOPC)对高糖基化终产物(AGEs)诱导的肝损伤的调节作用。在 Sprague Dawley(SD)雄性小鼠模型中,用正常 AIN-93G 饮食、高 AGEs 饮食(H)或 H 加 0.5 或 0.2%(w/w)LSOPC 喂养 12 周,建立了 LSOPC 的抗氧化特性模型。结果表明,LSOPC 通过抑制核转位 NF-κB 和 MAPK 信号通路的激活,抑制 AGEs 的形成,减轻 AGEs 诱导的肝损伤。此外,LSOPC 抑制肿瘤坏死因子-α(TNF-α)和白细胞介素 6(IL-6)基因的表达。综上所述,LSOPC 通过抑制 RAGE-MAPK-NF-κB 通路,可能抑制 AGEs 的形成,并通过长期饮食 AGEs 调节肝损伤。