MAPK/ERK通路
蛋白激酶B
氧化应激
胰岛素抵抗
p38丝裂原活化蛋白激酶
NF-κB
促炎细胞因子
化学
炎症
信号转导
肿瘤坏死因子α
免疫印迹
趋化因子
细胞生物学
药理学
胰岛素
内科学
生物
内分泌学
生物化学
医学
基因
作者
Zhenhua Liu,Mengke Wang,Yuhang Liu,Mengjie Ren,Xuefeng Xi,Shiming Li,Wenyi Kang
摘要
Patrinia scabiosaefolia, 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 P. scabiosaefolia 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-α 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-α, and IL-6. Western blot analysis showed that the significant inhibition of phosphorylation of IκB and P65 and P38, ERK and JNK suggested that the effects were exerted through NF-κB pathway and MAPK pathway. In 3 T3-L1 cells, patrinoside and patrinoside A also inhibited the activation of NF-κB and MAPK pathways through inhibiting the transcriptions of inflammatory cytokines IL-6 and chemokines MCP-1 and MIP-1α. 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-κB 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 P. scabiosaefolia.
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