Biomanufacturing Research Institute and Technology Enterprise, Durham, NC, USA.
Cell Mol Neurobiol. 2011 Jan;31(1):145-53. doi: 10.1007/s10571-010-9563-3. Epub 2010 Sep 17.
Past research has shown that natural products of plant and marine origins and their congeners enhance the actions of neuritogenic factors of the central nervous system (CNS) such as nerve growth factor (NGF). However, the role of fluorine substitutions in their structure-activity relationship (SAR) has not been explored. We have synthesized a trifluoromethyl analog of verbenachalcone (VC), a pharmacologically active natural compound previously shown to potentiate NGF activity. This analog, designated C278, enhances neurite outgrowth and proliferation of NeuroScreen-1™ (NS-1) cells, a subclone of PC12 pheochromocytoma cells. C278 increases the percentage of neurite bearing cells in the presence of suboptimal doses of NGF in comparison with controls treated with NGF alone. In addition, C278 stimulates cell growth in reduced serum and serum-free cell culture conditions based on our observation of increases in cell number and metabolic assessment with MTT reduction and resazurin assays. The addition of C278 partially restored inhibition of NGF-induced neurite outgrowth by the mitogen-activated protein kinase kinase (MEK) inhibitors PD98059 and U0126. Short-term sequential exposure of cells to U0126, C278, and NGF enhanced phosphorylation of extracellular signal-regulated kinase (ERK) in comparison with cells treated with only the MEK inhibitor and NGF. C278 also attenuated cell growth arrest caused by exposure to PD98059, U0126 and the phosphatidylinositol-3 kinase (PI3K) inhibitor, LY294002 but did not alter phosphorylation of Akt, a classic downstream target of PI3K during cell survival. These data suggest that C278 promotes NGF-dependent neurite outgrowth in NS-1 cells through a MEK signaling pathway by a mechanism that alters short-term activation of ERK. In contrast, C278 promotes PI3K-mediated survival independently of Akt phosphorylation.
过去的研究表明,植物和海洋来源的天然产物及其同系物增强了中枢神经系统(CNS)的神经营养因子(如神经生长因子(NGF))的作用。然而,氟取代在其结构-活性关系(SAR)中的作用尚未得到探索。我们合成了马鞭草素(VC)的三氟甲基类似物,VC 是一种先前被证明可增强 NGF 活性的具有药理活性的天然化合物。该类似物命名为 C278,可增强神经细胞(NeuroScreen-1™,NS-1)细胞的神经突生长和增殖,这是 PC12 嗜铬细胞瘤细胞的一个亚克隆。与单独用 NGF 处理的对照组相比,C278 在存在亚最佳剂量 NGF 的情况下增加了具有神经突的细胞的百分比。此外,根据我们观察到的细胞数量增加和 MTT 减少和 Resazurin 测定的代谢评估,C278 在减少血清和无血清细胞培养条件下刺激细胞生长。C278 部分恢复了丝裂原活化蛋白激酶激酶(MEK)抑制剂 PD98059 和 U0126 对 NGF 诱导的神经突生长的抑制。与仅用 MEK 抑制剂和 NGF 处理的细胞相比,细胞短期顺序暴露于 U0126、C278 和 NGF 可增强细胞外信号调节激酶(ERK)的磷酸化。C278 还减轻了 PD98059、U0126 和磷脂酰肌醇-3 激酶(PI3K)抑制剂 LY294002 暴露引起的细胞生长停滞,但不会改变 Akt 的磷酸化,Akt 是细胞存活过程中 PI3K 的经典下游靶点。这些数据表明,C278 通过改变 ERK 的短期激活,通过 MEK 信号通路促进 NS-1 细胞中 NGF 依赖性神经突生长。相比之下,C278 促进 PI3K 介导的存活而不依赖于 Akt 磷酸化。