丙泊酚对肝癌HepG2细胞侵袭的影响

Effects of Propofol on Hepatoma Carcinoma HepG2 Cell Invasion

目的:研究丙泊酚对肝癌Hep G2细胞侵袭的影响。方法:以0(阴性对照)、1、3、10μg/ml丙泊酚作用于肝癌Hep G2细胞48 h后,采用MTT法检测细胞活力,Transwell法检测细胞侵袭能力,Western blot法检测基质金属蛋白酶2(MMP-2)、MMP-9、E-钙黏附素(E-cadherin)、锌指转录因子(Snail)的表达及核因子-κB p65(NF-κB p65)磷酸化水平。结果:与阴性对照比较,1、3、10μg/ml丙泊酚能降低Hep G2细胞活力和侵袭能力,下调NF-κB p65磷酸化水平和Snail表达,上调E-cadherin表达(P<0.01);3、10μg/ml丙泊酚能下调MMP-2、MMP-9表达(P<0.01)。上述效果均呈浓度依赖性(P<0.01)。结论:丙泊酚能抑制肝癌Hep G2细胞侵袭,其机制可能与抑制NF-κB/Snail信号通路有关。

OBJECTIVE： To study the effects of propofol on invasion of hepatoma carcinoma HepG2 cell. METHODS： MTT method was used to detect the viability of HepG2 cells which were cultured with 0 （negative control）, 1, 3 and 10 μg/ml propofol for 48 h. The ability of cell invasion was detect by Tranaswell method. The phosphorylation level of nuclear factor-κB p65 （NF-κB p65） and the expression of matrix metalloproteinase 2 （MMP-2）, MMP-9, E-cadhherin and Snail were detected by Western blot method. RESULTS： Compared with negative control, 1, 3, 10μg/ml propofol inhibited the cell viability and invasion, down-regu- lated the expression of Snail and the phosphorylation level of NF-κB p65, and up-regulated the expression of E-cadherin （P〈 0.01 ）. 3, 10 μg/ml propofol down-regulated the expression of MMP-2 and MMP-9 （P〈0.01）. Above effects depended on drug con- centration （P〈 0.01 ）. CONCLUSIONS： Propofol can suppress HepG2 invasion, which might be related to the inhibition of NF-κB / Snail signal pathway.