摘要
目的:探讨丙泊酚对Hep G2肝母细胞瘤细胞侵袭能力的影响及相关机制。方法:用不同质量浓度(0、3、6、9和12 mg/L)丙泊酚培养Hep G2细胞24 h后,通过细胞侵袭实验检测侵袭率;培养24、48和72 h后用MTT法检测细胞活性;培养48 h后采用RT-PCR和Western blot法检测细胞中MMP-2、MMP-9 mRNA及MMP-2、MMP-9和TIMP-1蛋白的表达。结果:随丙泊酚质量浓度的增加,Hep G2细胞的侵袭能力逐渐降低(F=4 883.900,P<0.001),细胞活性逐渐降低(F=38.334,P<0.001),MMP-2及MMP-9 mRNA及蛋白的表达亦逐渐降低(P<0.05),而TIMP-1蛋白的表达逐渐升高(F=44.918,P<0.001)。结论:丙泊酚能降低Hep G2细胞的侵袭能力及细胞活性,其机制与抑制MMP-2和MMP-9蛋白的表达及促进TIMP-1蛋白的表达有关。
Aim: To investigate the effects and related mechanism of propofol on the invasion ability of Hep G2 cells.Methods: Different concentrations( 0,3,6,9 and 12 mg / L) of propofol were used to treat Hep G2 cells. The invasion ability was detected by Transwell after 24 h treatment; cell viability of Hep G2 cells was studied through MTT assay after 24,48,and 72 h treatment. The expressions of MMP-2,MMP-9 and TIMP-1 were measured through RT-PCR and Western blot after48 h treatment. Results: The invasion ability and cell viability of Hep G2 cells,the mRNA and protein expressions of MMP-2 and MMP-9,were significantly decreased with the increase of propofol concentration( P〈0. 05). The protein expression of TIMP-1 was significantly increased with the increase of propofol concentration( F = 44. 918, P〈0. 001). Conclusion: Propofol could reduce the invasive activity and cell viability of Hep G2 cells through the inhibition of MMP-2 and MMP-9,and overexpression of TIMP-1.
出处
《郑州大学学报(医学版)》
CAS
北大核心
2015年第3期318-322,共5页
Journal of Zhengzhou University(Medical Sciences)
基金
国家自然科学基金青年项目81301308
81301040
陕西省自然科学基础研究计划项目2014JQ4158
陕西省青年科技新星项目2014KJXX-76