National R & D Center for Edible Fungus Processing Technology, Henan University, Kaifeng 475004, China.
Functional Food Engineering Technology Research Center, Henan, Kaifeng 475004, China.
Oxid Med Cell Longev. 2023 Jan 24;2023:9069645. doi: 10.1155/2023/9069645. eCollection 2023.
, as traditional food and medicine plant, was used to treat appendicitis, enteritis, and hepatitis for thousand years in China. Patrinoside and patrinoside A isolated from could significantly improve insulin resistance (IR) by activating PI-3 K/AKT signaling pathway in our previous study. Since IR is closely related to inflammation, their anti-inflammatory activities in RAW264.7 inflammatory model induced by LPS and in 3 T3-L1 IR inflammatory model induced by TNF- were evaluated to identify whether the effects on improving IR related to anti-inflammatory activity. In RAW264.7 cells, patrinoside and patrinoside A significantly inhibited the transcription and secretion of inflammatory mediators NO, TNF-, and IL-6. Western blot analysis showed that the significant inhibition of phosphorylation of IB and P65 and P38, ERK and JNK suggested that the effects were exerted through NF-B pathway and MAPK pathway. In 3 T3-L1 cells, patrinoside and patrinoside A also inhibited the activation of NF-B and MAPK pathways through inhibiting the transcriptions of inflammatory cytokines IL-6 and chemokines MCP-1 and MIP-1. These events resulted in the inhibition of macrophages migration to adipocytes. In addition, patrinoside and patrinoside A ameliorated oxidative stress by inhibiting ROS release in LPS-stimulated RAW264.7 cells. In conclusion, patrinoside and patrinoside A could active PI-3 K/AKT pathway, inhibit NF-B pathway, MAPK pathway, and improve oxidative stress, which showed multipathways on improving IR. These results provided the scientific basis for material basis and mechanism on improving IR of .
作为传统的食物和药材,在中国被用于治疗阑尾炎、肠炎和肝炎已有千年历史。我们之前的研究发现,从 中分离得到的帕特里诺苷和帕特里诺苷 A 通过激活 PI-3K/AKT 信号通路,能显著改善胰岛素抵抗(IR)。由于 IR 与炎症密切相关,因此评估了它们在 LPS 诱导的 RAW264.7 炎症模型和 TNF-α诱导的 3T3-L1 IR 炎症模型中的抗炎活性,以确定改善 IR 的作用是否与抗炎活性有关。在 RAW264.7 细胞中,帕特里诺苷和帕特里诺苷 A 显著抑制了炎症介质 NO、TNF-α和 IL-6 的转录和分泌。Western blot 分析表明,IB 和 P65、P38、ERK 和 JNK 的磷酸化显著抑制,表明作用是通过 NF-B 途径和 MAPK 途径发挥的。在 3T3-L1 细胞中,帕特里诺苷和帕特里诺苷 A 也通过抑制炎症细胞因子 IL-6 和趋化因子 MCP-1 和 MIP-1 的转录,抑制 NF-B 和 MAPK 途径的激活,从而抑制巨噬细胞向脂肪细胞的迁移。此外,帕特里诺苷和帕特里诺苷 A 通过抑制 LPS 刺激的 RAW264.7 细胞中 ROS 的释放,改善了氧化应激。总之,帕特里诺苷和帕特里诺苷 A 可以激活 PI-3K/AKT 通路,抑制 NF-B 通路、MAPK 通路,改善氧化应激,这表明在改善 IR 方面具有多途径作用。这些结果为改善 的物质基础和机制提供了科学依据。