caffeic acid anhydride | 945404-43-3

• 分子结构分类: 有机化合物 - 苯丙烷和聚酮 - 肉桂酸及其衍生物
• 英文名称: caffeic acid anhydride
• 英文别名: caffeic anhydride；(2E)-3-(3,4-dihydroxyphenyl)prop-2-enoyl (2E)-3-(3,4-dihydroxyphenyl)prop-2-enoate；3-(3,4-dihydroxyphenyl)prop-2-enoyl 3-(3,4-dihydroxyphenyl)prop-2-enoate
• CAS: 945404-43-3
• 化学式: C₁₈H₁₄O₇
• 分子量: 342.305
• InChiKey: QDPOOGQUCJJZAO-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  2.6
• 重原子数：
  25
• 可旋转键数：
  6
• 环数：
  2.0
• sp3杂化的碳原子比例：
  0.0
• 拓扑面积：
  124
• 氢给体数：
  4
• 氢受体数：
  7

反应信息

• 作为反应物：
  描述：

  caffeic acid anhydride 、 甲基色氨酸 反应 12.0h， 生成 methyl (E)-(3-(3,4-dihydroxyphenyl)acryloyl)tryptophanate
  参考文献：
  名称：

  Methyl (E)-(3-(3,4-dihydroxyphenyl)acryloyl)tryptophanate can suppress MCP-1 expression by inhibiting p38 MAP kinase and NF-κB in LPS-stimulated differentiated THP-1 cells

  摘要：

  Methyl (E)-(3-(3,4-dihydroxyphenyl)acryloyl)tryptophanate (MHAT) is an O-methyl ester of javamide-II showing strong anti-inflammatory activity. Therefore, in this study, MHAT was chemically synthesized, and its effects on p38 MAP kinase, NF-kappa B, and monocyte chemotactic factor-1 (MCP-1) expression were investigated in LPS-stimulated differentiated THP-1 cells. MHAT inhibited p38 MAP kinase with an IC50 of 12 mu M, and the inhibition was supported by an in silico model showing that its binding to p38 MAP kinase was stronger than that of SB203580. At the concentration of 20 mu M, the p38 inhibition reduced ATF-2 phosphorylation by 55% (P < 0.05). Additionally, MHAT inhibited NF-kappa B (p65) phosphorylation by 30% (P < 0.05) at the same concentration, suggesting that MHAT was able to reduce NF-kappa B transcriptional activity. This supposition was confirmed by the NF-kappa B reporter assay, demonstrating that MHAT (20 mu M) could suppress NF-kappa B transcriptional activity by 29% (P < 0.05) in the NF-kappa B reporter (Luc)-HEK293 cell line. As expected, the treatment with MHAT (5-40 mu M) significantly inhibited MCP-1 mRNA expression by 9-73% (P < 0.05) and the production of MCP-1 protein by 10-70% (P < 0.05) in the THP-1 cells. Furthermore, MHAT was found to inhibit RANTES expression as well in the same THP-1 cells, supporting its purported inhibition of p38 MAP kinase and NF-kappa B. All these data suggest that MHAT is a potent compound that can inhibit MCP-1 production by suppressing p38 kinase/ATF-2 phosphorylation and NF-kappa B in the differentiated THP-1 cells.

  DOI：

  10.1016/j.ejphar.2017.07.006
• 作为产物：
  描述：

  咖啡酸 在 N,N'-二异丙基碳二亚胺 作用下， 以 二甲基亚砜 为溶剂， 生成 caffeic acid anhydride
  参考文献：
  名称：

  Methyl (E)-(3-(3,4-dihydroxyphenyl)acryloyl)tryptophanate can suppress MCP-1 expression by inhibiting p38 MAP kinase and NF-κB in LPS-stimulated differentiated THP-1 cells

  摘要：

  Methyl (E)-(3-(3,4-dihydroxyphenyl)acryloyl)tryptophanate (MHAT) is an O-methyl ester of javamide-II showing strong anti-inflammatory activity. Therefore, in this study, MHAT was chemically synthesized, and its effects on p38 MAP kinase, NF-kappa B, and monocyte chemotactic factor-1 (MCP-1) expression were investigated in LPS-stimulated differentiated THP-1 cells. MHAT inhibited p38 MAP kinase with an IC50 of 12 mu M, and the inhibition was supported by an in silico model showing that its binding to p38 MAP kinase was stronger than that of SB203580. At the concentration of 20 mu M, the p38 inhibition reduced ATF-2 phosphorylation by 55% (P < 0.05). Additionally, MHAT inhibited NF-kappa B (p65) phosphorylation by 30% (P < 0.05) at the same concentration, suggesting that MHAT was able to reduce NF-kappa B transcriptional activity. This supposition was confirmed by the NF-kappa B reporter assay, demonstrating that MHAT (20 mu M) could suppress NF-kappa B transcriptional activity by 29% (P < 0.05) in the NF-kappa B reporter (Luc)-HEK293 cell line. As expected, the treatment with MHAT (5-40 mu M) significantly inhibited MCP-1 mRNA expression by 9-73% (P < 0.05) and the production of MCP-1 protein by 10-70% (P < 0.05) in the THP-1 cells. Furthermore, MHAT was found to inhibit RANTES expression as well in the same THP-1 cells, supporting its purported inhibition of p38 MAP kinase and NF-kappa B. All these data suggest that MHAT is a potent compound that can inhibit MCP-1 production by suppressing p38 kinase/ATF-2 phosphorylation and NF-kappa B in the differentiated THP-1 cells.

  DOI：

  10.1016/j.ejphar.2017.07.006