夏枯草水提取物对血管平滑肌细胞增殖的影响及其机制研究

目的:探讨夏枯草水提取物对血管紧张素II诱导的血管平滑肌细胞（vascular smooth muscle cells，VSMCs）增殖作用及对Daxx/PTEN/NF-κB信号通路的影响。方法:培养VSMCs，体外用血管紧张素II （angiotensin II,Ang-II）(1 μmol/L)诱导细胞增殖模型，MTT和BrdU法分别检测夏枯草水提取物不同浓度(10、20、40、80、160 μg/mL)作用24 h后对VSMCs活性和增殖的影响、划痕法观察细胞迁移力，Western blot检测细胞中Daxx、PTEN、NF-κB蛋白表达。结果:与对照组比较，模型组VSMCs活力及细胞迁移能力明显增强；同时细胞中Daxx、PTEN蛋白表达明显降低，NF-κB蛋白显著上调；与模型组比较，20、40、80 μg/mL夏枯草水提取物成浓度依赖性显著抑制VSMCs活力与细胞迁移能力，以80 μg/mL浓度最显著；同时，夏枯草水提取物处理组细胞Daxx、PTEN蛋白表达明显上调，NF-κB蛋白下调。结论:夏枯草水提取物能显著抑制Ang-II诱导的VSMCs增殖与迁移，其机制可能与Daxx/PTEN/NF-κB信号通路有关。

Roles of Prunella vulgaris L. in the proliferation and migration of vascular smooth muscle cells and its molecular mechanisms

AIM: To investigate the effects of Prunella vulgaris L. (PV) on Ang II-induced proliferation of VSMCs and the effect of Daxx/PTEN/NF-κB signaling pathway. METHODS: The VSMCs line was cultured, and the cell proliferation model was induced by Ang-II (1 μmol/L) in vitro. The MTT and BrdU methods were used to detect the effects of VSMCs activity and proliferation by different concentrations of PV (10, 20, 40, 80,160 μg/mL) for 24 h. Cell migration was observed by scratch method, and Daxx, PTEN and NF-κB protein expression was detected by Western blot. RESULTS:Compared with the control group, the viability and cell migration ability of VSMCs in the model group were significantly enhanced. At the same time, the expression of Daxx and PTEN protein was significantly decreased, and the NF-κB protein was significantly up-regulated.Compared with the model group, PV (20, 40, 80 μg/mL) significantly inhibited VSMCs viability and cell migration ability in a concentration-dependent manner, with the most significant concentration at 80 μg/mL.Meanwhile, the expression of Daxx and PTEN protein were significantly up-regulated and NF-κB protein was down-regulated in VSMCs treated by PV. CONCLUSION: PV can inhibit the proliferation and migration of VSMCs induced by Ang-II , and the mechanism may be associated with increasing expression of Daxx and PTEN, inhibiting expression of NF-κB.