肉桂醛对神经胶质瘤U251细胞生物学行为的影响

目的 探讨肉桂醛对胶质瘤细胞生物学行为的影响及其分子机制。方法 体外培养胶质瘤细胞系U251细胞，分为对照组、低剂量肉桂醛组（40 μmol/L）和高剂量肉桂醛组（80 μmol/L）。采用平板克隆和CCK-8试验检测细胞增殖水平；流式细胞术分析细胞凋亡率；Transwell小室实验和细胞划痕试验评估细胞迁移和侵袭水平；免疫印迹法分析凋亡相关蛋白、PI3K/Akt和Wnt/β-catenin通路相关蛋白表达。结果 肉桂醛明显抑制胶质瘤U251细胞增殖、侵袭、迁移能力（P<0.05），促进细胞凋亡（P<0.05）；抑制Bcl-2、p-PI3K、p-Akt、 cycling D、C-Myc、β-catenin表达（P<0.05），促进Cleaved-Caspase-3、Bax表达（P<0.05）；而且，随剂量增大，肉桂醛的作用明显增强（P<0.05）。结论 肉桂醛抑制胶质瘤细胞增殖、侵袭、迁移，促进细胞凋亡，其机制可能与下调PI3K/Akt和Wnt/β-catenin信号通路有关。

Effect of cinnamaldehyde on the malignant biological behavior of glioma U251 cells

Objective To study the effect of cinnamaldehyde (CA) on the malignant biological behavior of glioma cells and its possible molecular mechanism. Methods The glioma U251 cells were cultured in vitro and divided into three groups, i.e., control group, low-dose CA group (40 μmol/L), and high-dose CA group (80 μmol/L). Plate cloning and CCK-8 experiments were used to detect the proliferation of U251 cells. Flow cytometry was used to analyze the apoptosis rate of U251 cells. Transwell assay and cell scratch assay were used to analyze the invasion and migration of U251 cells. Western blotting was used to analyze the protein expression of PI3K/Akt and Wnt/β-catenin pathway. Results CA significantly inhibited the proliferation, invasion and migration of glioma U251 cells (P<0.05), and significantly promoted cell apoptosis (P<0.05). CA significantly inhibited the expression of Bcl-2, p-PI3K, p-Akt, Cycling D, c-Myc and β-catenin (P<0.05), and significantly promoted the expression of Cleaved caspase-3 and Bax (P<0.05). The effect of CA on U251 cells was significantly enhanced with the dose increasing (P<0.05). Conclusions CA can inhibit the proliferation, invasion and migration of glioma cells and promote cell apoptosis, which may be related to the down-regulation of PI3K/Akt and Wnt/β-catenin signaling pathways.