罗哌卡因调控PI3K/Akt信号通路影响宫颈癌细胞HeLa的生物学行为

Ropivacaine affects the biological behavior of cervical cancer cells HeLa by regulating PI3K/Akt signal pathway

目的探讨罗哌卡因对宫颈癌细胞增殖、迁移侵袭和凋亡的影响和分子机制。方法细胞计数试剂盒(CCK-8)法检测不同浓度罗哌卡因对HeLa细胞增殖活力的影响,筛选最佳用药浓度。Transwell法、流式细胞术检测细胞迁移侵袭和凋亡;蛋白质印记(Western blot)检测细胞增殖、迁移、侵袭、凋亡以及磷脂酰肌醇3-激酶(PI3K)/蛋白激酶B(Akt)信号通路相关蛋白的表达水平。结果与0μg/mL组比较,罗哌卡因100、200和400μg/mL组HeLa细胞增殖活力显著降低。随着给药剂量的增加,HeLa细胞的增殖活力逐渐降低(P<0.05);与对照组比较,罗哌卡因处理组(400μg/mL)HeLa细胞的迁移和侵袭能力、p-Akt表达水平显著降低,细胞凋亡率显著升高,差异均有统计学意义(P<0.05)。结论罗哌卡因可抑制宫颈癌细胞增殖、迁移和侵袭,诱导细胞凋亡,其机制可能是通过抑制PI3K/Akt信号通路实现的。

Objective To investigate the effect and molecular mechanism of ropivacaine on proliferation,migration,invasion and apoptosis of cervical cancer cells. Methods Cell counting kit(CCK-8)was used to detect the effects of ropivacaine with different concentrations on the proliferation activity of He La cells to selecte the optimal drug concentration. Transwell assay and flow cytometry were used to detect cell migration,invasion and apoptosis;Western blot was used to detect the expression levels of cell proliferation,migration,invasion,apoptosis and phosphoinositide 3-kinase(PI3 K)/protein kinase B(Akt)signaling pathway-related proteins.Results Compared with the 0 μg/m L group,the proliferation activity of He La cells in the 100,200 and 400 μg/m L ropivacaine groups was significantly reduced. With the increase of dose,the proliferation activity of He La cells decreased gradually(P < 0. 05). Compared with the control group,the migration and invasion ability,p-Akt expression level of He La cells in the ropivacaine treatment group(400 μg/m L)was significantly decreased,the apoptosis rate was significantly increased(P < 0. 05). Conclusion Ropivacaine inhibits the proliferation,migration and invasion of cervical cancer cells and promotes apoptosis,which may be realized by inhibiting the PI3 K/Akt signaling pathway.