Department of Pharmacology, Faculty of Pharmacy, Takasaki University of Health and Welfare, Gunma, Japan.
Department of Natural Medicines, Faculty of Pharmacy, Takasaki University of Health and Welfare, Gunma, Japan.
Pharmazie. 2024 May 15;79(3):67-71. doi: 10.1691/ph.2024.3656.
We examined the mechanism by which 24()-ethyllophenol (MAB28) isolated from the branches of caused neurite outgrowth in rat pheochromocytoma cells (PC12). MAB28 significantly promoted neurite outgrowth to a similar degree as the positive control, nerve growth factor (NGF). After incubation with MAB28 in PC12 cells, phosphorylation of extracellular signal-regulated kinase, p38 mitogen-activated protein kinase, and cyclic AMP response element-binding protein was detected, but the time course of phosphorylation was different from that induced by NGF. The expression of chloride intracellular channel protein 3 (CLIC3) was significantly decreased by MAB28. 5-Nitro-2-(3-phenylpropylamino)-benzoic acid (NPPB), an outward rectifying chloride channel inhibitor, significantly promoted neurite outgrowth in PC12 cells. These data suggested that MAB28 could induce neurite outgrowth by downregulating CLIC3 expression.
我们研究了 24()-ethyllophenol (MAB28) 从枝条中分离出来的机制，这种物质能够促进大鼠嗜铬细胞瘤细胞 (PC12) 的轴突生长。MAB28 显著促进轴突生长的程度与阳性对照物神经生长因子 (NGF) 相当。在 PC12 细胞中用 MAB28 孵育后，检测到细胞外信号调节激酶、p38 丝裂原激活蛋白激酶和环磷酸腺苷反应元件结合蛋白的磷酸化，但磷酸化的时间进程与 NGF 诱导的不同。MAB28 显著降低氯离子通道蛋白 3 (CLIC3) 的表达。5-硝基-2-(3-苯丙基氨基)-苯甲酸 (NPPB)，一种外向整流氯离子通道抑制剂，显著促进 PC12 细胞的轴突生长。这些数据表明，MAB28 可以通过下调 CLIC3 的表达来诱导轴突生长。
