Inhibition of advanced glycation endproducts formation by lotus seedpod oligomeric procyanidins through RAGE-MAPK signaling and NF-kappa B activation in high-AGEs-diet mice
Inhibition of advanced glycation endproducts formation by lotus seedpod oligomeric procyanidins through RAGE-MAPK signaling and NF-kappa B activation in high-AGEs-diet mice
复制标题
莲蓬寡聚原花青素通过 RAGE-MAPK 信号传导和 NF-κ B 激活抑制高 AGEs 饮食小鼠中晚期糖基化终产物的形成
DOI：
10.1016/j.fct.2021.112481
复制
发表时间：
2021
影响因子：
4.3
通讯作者：
Zhou Mengzhou
中科院分区：
文献类型：
--
作者：
Wu Qian;Feng Yingna;Ouyang Yu;Liang Yinggang;Zhao Kuoquan;Wang Ying;Luo Qing;Xiao Juan;Feng Nianjie;Zhou Mengzhou
本研究在小鼠模型中探讨莲蓬寡聚原花青素 (LSOPC) 通过晚期糖基化终末产物受体 (RAGE)-丝裂原激活蛋白激酶 (MAPK)-核因子-κB (NF-κB) 信号通路对晚期糖基化终末产物 (AGE) 诱导的肝损伤的调节作用。为了检查 LSOPC 的抗氧化特性，使用 Sprague Dawley (SD) 雄性小鼠建立了高 AGEs 饮食模型，这些小鼠喂食正常 AIN-93G 饮食、高 AGEs 饮食 (H) 或 H 加 0.5 或 0.2% (w/w) LSOPC 12 周。我们的结果表明，LSOPC 通过抑制 NF-κB 的核转位和 MAPK 信号通路的激活来抑制 AGEs 形成并减轻 AGEs 诱导的肝损伤。此外，LSOPC 还能抑制肿瘤坏死因子-α (TNF-α) 和白细胞介素 6 (IL-6) 的基因表达。综上所述，LSOPC 治疗可能抑制 AGE 形成，并通过抑制 RAGE-MAPK–NF–κB 途径，通过长期饮食 AGE 调节肝损伤。
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.