(E)-3-[4-[(2S,3R,4S,5R,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)oxan-2-yl]oxyphenyl]prop-2-enal

• 分子结构分类: 有机化合物 - 有机氧化合物
• 英文名称: (E)-3-[4-[(2S,3R,4S,5R,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)oxan-2-yl]oxyphenyl]prop-2-enal
• 化学式: C₁₅H₁₈O₇
• 分子量: 310.304
• InChiKey: XPOUAEZWSDWKBT-WEHGBGHESA-N

计算性质

• 辛醇/水分配系数(LogP)：
  0
• 重原子数：
  22
• 可旋转键数：
  5
• 环数：
  2.0
• sp3杂化的碳原子比例：
  0.4
• 拓扑面积：
  116
• 氢给体数：
  4
• 氢受体数：
  7

反应信息

• 作为产物：
  描述：

  2,3,4,6-四-O-乙酰基-Alpha-D-吡喃半乳糖酰基-2,2,2-三氯代亚氨乙酸酯 在 三氟化硼乙醚 、 potassium tert-butylate 、 sodium methylate 作用下， 以 四氢呋喃 、 甲醇 、 二氯甲烷 为溶剂， 反应 27.0h， 生成 (E)-3-[4-[(2S,3R,4S,5R,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)oxan-2-yl]oxyphenyl]prop-2-enal
  参考文献：
  名称：

  A low toxicity synthetic cinnamaldehyde derivative ameliorates renal inflammation in mice by inhibiting NLRP3 inflammasome and its related signaling pathways

  摘要：

  Uncontrolled inflammation is a leading cause of various chronic diseases. Cinnamaldehyde (CA) is a major bioactive compound isolated from the essential oil of the leaves of Cinnamomum osmophloeum kaneh that exhibits anti-inflammatory activity; however, the use of CA is limited by its cytotoxicity. Here, we synthesized three CA derivatives and identified 4-hydroxycinnamaldehyde-galactosamine (HCAG) as a low toxicity anti-inflammatory compound in vitro (HCAG IC50 >> 1600 mu M; CA IC50=40 mu M) and in vivo. HCAG reduced pro-inflammatory mediator expression in LPS-activated macrophages by inhibiting MAPK and PKC-alpha/delta phosphorylation, decreasing ROS generation and reducing NF-kappa B activation. HCAG also reduced NLRP3 inflammasome-derived IL-1 beta secretion by inhibiting the ATP-mediated phosphorylation of AKT and PKC-alpha/delta. In a mouse model of LPS-induced renal inflammation, we observed reduced albuminuria and a mild degree of glomerular proliferation, glomerular sclerosis and periglomerular inflammation in the HCAG-treated mice compared with the vehicle-treated mice. The underlying mechanisms for these renoprotective effects involved: (1) inhibited NLRP3 inflammasome activation; (2) decreased superoxide anion levels and apoptosis; and (3) suppressed activation of NF-kappa B and related downstream inflammatory mediators. (C) 2015 Elsevier Inc. All rights reserved.

  DOI：

  10.1016/j.freeradbiomed.2015.12.003

文献信息

• A low toxicity synthetic cinnamaldehyde derivative ameliorates renal inflammation in mice by inhibiting NLRP3 inflammasome and its related signaling pathways
  作者：Shuk-Man Ka、Louis Kuoping Chao、Jung-Chen Lin、Shui-Tein Chen、Wen-Tai Li、Chien-Nan Lin、Jen-Che Cheng、Huei-Ling Jheng、Ann Chen、Kuo-Feng Hua

  DOI：10.1016/j.freeradbiomed.2015.12.003

  日期：2016.2

  Uncontrolled inflammation is a leading cause of various chronic diseases. Cinnamaldehyde (CA) is a major bioactive compound isolated from the essential oil of the leaves of Cinnamomum osmophloeum kaneh that exhibits anti-inflammatory activity; however, the use of CA is limited by its cytotoxicity. Here, we synthesized three CA derivatives and identified 4-hydroxycinnamaldehyde-galactosamine (HCAG) as a low toxicity anti-inflammatory compound in vitro (HCAG IC50 >> 1600 mu M; CA IC50=40 mu M) and in vivo. HCAG reduced pro-inflammatory mediator expression in LPS-activated macrophages by inhibiting MAPK and PKC-alpha/delta phosphorylation, decreasing ROS generation and reducing NF-kappa B activation. HCAG also reduced NLRP3 inflammasome-derived IL-1 beta secretion by inhibiting the ATP-mediated phosphorylation of AKT and PKC-alpha/delta. In a mouse model of LPS-induced renal inflammation, we observed reduced albuminuria and a mild degree of glomerular proliferation, glomerular sclerosis and periglomerular inflammation in the HCAG-treated mice compared with the vehicle-treated mice. The underlying mechanisms for these renoprotective effects involved: (1) inhibited NLRP3 inflammasome activation; (2) decreased superoxide anion levels and apoptosis; and (3) suppressed activation of NF-kappa B and related downstream inflammatory mediators. (C) 2015 Elsevier Inc. All rights reserved.