布比卡因对肝癌HepG2细胞增殖、侵袭和凋亡及miR-191/KLF6信号轴的影响

Effects of bupivacaine on the proliferation,invasion,apoptosis and miR-191/KLF6 signal axis of hepatocellular carcinoma HepG2 cells

目的:探讨布比卡因对肝癌HepG2细胞增殖、侵袭、凋亡及微小RNA-191(miR-191)/Krüppel样因子6(KLF6)信号轴的影响。方法:设肝癌HepG2细胞组、顺铂组(3.0μg/ml)、布比卡因低剂量组(2.5 mg/ml)、布比卡因高剂量组(5.0 mg/ml)。培养72 h后,测定肝癌HepG2细胞存活率、穿膜数、凋亡率、miR-191、KLF6 mRNA和蛋白水平。结果:与肝癌HepG2细胞组比较,顺铂组、布比卡因低、高剂量组肝癌HepG2细胞存活率、穿膜数、miR-191水平降低,凋亡率、KLF6 mRNA和蛋白水平升高(P<0.05);与顺铂组比较,布比卡因低、高剂量组肝癌HepG2细胞存活率、穿膜数、miR-191水平升高,凋亡率、KLF6 mRNA和蛋白水平降低(P<0.05);与布比卡因低剂量组比较,布比卡因高剂量组肝癌HepG2细胞存活率、穿膜数、miR-191水平降低,凋亡率、KLF6 mRNA和蛋白水平升高(P<0.05)。结论:布比卡因能明显抑制肝癌HepG2细胞增殖和侵袭,促进其凋亡;其机制可能与布比卡因降低肝癌HepG2细胞中miR-191的表达进而促进KLF6的表达有关。

Objective:To investigate the effects of bupivacaine on proliferation,invasion,apoptosis and microRNA-191(miR-191)/Krüppel-like factor 6(KLF6)signal axis in hepatocellular carcinoma HepG2 cells.Methods:Hepatocellular carcinoma HepG2 cells group,cisplatin group(3μg/mL),bupivacaine low dose group(2.5 mg/mL),bupivacaine high dose group(5 mg/mL)were set for the research.After 72 hours of incubation,the survival rate,number of penetrating membrane,apoptosis rate,miR-191,KLF6 mRNA and protein levels of hepatocellular carcinoma HepG2 cells were determined.Results:Compared with hepatocellular carcinoma HepG2 cells group,the survival rate,number of penetrating membrane and miR-191 level of hepatocellular carcinoma HepG2 cells in cisplatin group,bupivacaine low dose group and bupivacaine high dose group were decreased,while the apoptosis rate,KLF6 mRNA and protein level were increased(P<0.05).Compared with cisplatin group,the survival rate,number of penetrating membrane and miR-191 level of hepatocellular carcinoma HepG2 cells in bupivacaine low and high dose groups were increased,while the apoptosis rate,KLF6 mRNA and protein level were decreased(P<0.05).Compared with bupivacaine low dose group,the survival rate,number of penetrating membrane and miR-191 level of hepatocellular carcinoma HepG2 cells in bupivacaine high dose group were decreased,while the apoptosis rate,KLF6 mRNA and protein level were increased(P<0.05).Conclusion:Bupivacaine can significantly inhibit the proliferation and invasion of hepatocellular carcinoma HepG2 cells and promote apoptosis.The efficacy may be related to the reduction of miR-191 expression in hepatocellular carcinoma HepG2 cells by bupivacaine and thus promote the expression of KLF6.