去氧穿心莲内酯 | 79233-15-1

• 物质功能分类: 生物化工 - 提取物
• 分子结构分类: 有机化合物 - 脂质和类脂质分子 - 异戊烯醇脂质
• 中文名称: 去氧穿心莲内酯
• 中文别名: 穿心莲甲素；n14-去氧穿心莲内酯；14-去氧穿心莲内酯
• 英文名称: deoxyandrographolide
• 英文别名: 4-[2-[(4aS,5R,6R,8aR)-6-hydroxy-5-(hydroxymethyl)-2,5,8a-trimethyl-3,4,4a,6,7,8-hexahydronaphthalen-1-yl]ethyl]-2H-furan-5-one
• CAS: 79233-15-1
• 化学式: C₂₀H₃₀O₄
• 分子量: 334.456
• InChiKey: DAXSYTVXDSOSIE-HNJRGHQBSA-N

物化性质

• 沸点：
  511.7±50.0 °C(Predicted)
• 密度：
  1.123±0.06 g/cm3(Predicted)

计算性质

• 辛醇/水分配系数(LogP)：
  2.9
• 重原子数：
  24
• 可旋转键数：
  4
• 环数：
  3.0
• sp3杂化的碳原子比例：
  0.75
• 拓扑面积：
  66.8
• 氢给体数：
  2
• 氢受体数：
  4

制备方法与用途

作用

去氧穿心莲内酯是常用中药穿心莲的有效成分之一，是从穿心莲中分离得到的一种二萜内酯类化合物。现代药理学研究表明，去氧穿心莲内酯具有解热、抗炎、抗钩端螺旋体病、抗菌、抗癌、保肝作用和抗高血压等活性。

应用

去氧穿心莲内酯具有抗菌和抗钩端螺旋体的作用。临床试用于治疗钩端螺旋体、急性细菌性痢疾、上呼吸道感染、流行性感冒及原因不明的发热等病症，均有一定的疗效。毒性小，未见明显副作用。它能够减少二甲苯或H+刺激所致伊文思兰自毛细血管壁的渗出，具有抑制巴豆油所致大鼠炎性渗出的作用，并对大鼠蛋清性足肿有显著抑制作用。此外，还表现出对肾上腺皮质功能不同程度的兴奋作用。

生物活性

Deoxyandrographolide 分离自穿心莲中，可抑制 LPS 诱导的 iNOS mRNA 水平升高及促炎症介质 TNF-α 和 IL-6 的产生。同时，它还能增强 NGF 诱导的神经突起生长。

化学性质

去氧穿心莲内酯是一种白色结晶粉末，能够溶于甲醇、乙醇、DMSO 等有机溶剂，来源于穿心莲 Andrographis paniculata (Burm. f.) Nees。

用途

主要用于含量测定、鉴定及药理实验等。

反应信息

• 作为产物：
  描述：

  3,19-diacetyl-14-deoxyandrographolide 在 盐酸 作用下， 以 甲醇 为溶剂， 反应 1.5h， 以21.6%的产率得到去氧穿心莲内酯
  参考文献：
  名称：

  Synthesis of andrographolide analogues and their neuroprotection and neurite outgrowth-promoting activities

  摘要：

  Alzheimer's disease (AD) is the most prevalent neurodegenerative disease and remains incurable. Currently, neuronal injury and synapse loss have been considered to be main features in the pathophysiology of AD. Thus, modulation of neuronal survival and neurite outgrowth may represent an efficient strategy for the treatment of AD. Based on the isolates from the traditional medicine Andrographis paniculata, a series of andrographolide analogues were prepared and evaluated for the neuroprotection and neurotrophic activity. Two compounds (3 and 12) could effectively inhibit LPS-induced NO production and iNOS expression as well as proinflammatory cytokines TNF-alpha and IL-6. Moreover, pretreatment with 3 and 12 could protect neurons against microgli-amediated neurotoxicity. Further, H2O2- and 6-OHDA induced neurotoxicity in PC12 cells were also attenuated by the novel 12. Our next study indicated that compounds 1, 4 and 10 promoted NGF-induced neurite outgrowth in PC12 cells, with 10 the most potent. To clarify the underlying mechanisms of active compounds (3, 10 and 12), system pharmacology was employed. The results revealed that muscarinic acetylcholine receptors (mAChRs) may be the main targets of 12 against AD, while thyroid hormone signaling pathway was involved in the mechanisms of 10. These study point to the therapeutic potential of andrographolide analogues against AD.

  DOI：

  10.1016/j.bmc.2019.04.025

文献信息

• Fujita, Tetsuro; Fujitani, Ryujiro; Takeda, Yoshio, Chemical and pharmaceutical bulletin, 1984, vol. 32, # 6, p. 2117 - 2125
  作者：Fujita, Tetsuro、Fujitani, Ryujiro、Takeda, Yoshio、Takaishi, Yoshihisa、Yamada, Toshihide、et al

  DOI：——

  日期：——
• Synthesis of andrographolide analogues and their neuroprotection and neurite outgrowth-promoting activities
  作者：Yuanzhen Xu、Hongbo Wei、Jianping Wang、Weiwei Wang、Jinming Gao

  DOI：10.1016/j.bmc.2019.04.025

  日期：2019.6

  Alzheimer's disease (AD) is the most prevalent neurodegenerative disease and remains incurable. Currently, neuronal injury and synapse loss have been considered to be main features in the pathophysiology of AD. Thus, modulation of neuronal survival and neurite outgrowth may represent an efficient strategy for the treatment of AD. Based on the isolates from the traditional medicine Andrographis paniculata, a series of andrographolide analogues were prepared and evaluated for the neuroprotection and neurotrophic activity. Two compounds (3 and 12) could effectively inhibit LPS-induced NO production and iNOS expression as well as proinflammatory cytokines TNF-alpha and IL-6. Moreover, pretreatment with 3 and 12 could protect neurons against microgli-amediated neurotoxicity. Further, H2O2- and 6-OHDA induced neurotoxicity in PC12 cells were also attenuated by the novel 12. Our next study indicated that compounds 1, 4 and 10 promoted NGF-induced neurite outgrowth in PC12 cells, with 10 the most potent. To clarify the underlying mechanisms of active compounds (3, 10 and 12), system pharmacology was employed. The results revealed that muscarinic acetylcholine receptors (mAChRs) may be the main targets of 12 against AD, while thyroid hormone signaling pathway was involved in the mechanisms of 10. These study point to the therapeutic potential of andrographolide analogues against AD.