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目的观察 VK2对 MHCC97H 细胞在生长、黏附、侵袭、凋亡以及 Caspase-3活性的影响。方法噻唑蓝(MTT)法检测细胞生长;体外细胞黏附及侵袭实验检测细胞的黏附和侵袭能力;Annexin V-FITC Apoptosis Detection K 和 Caspase-3 Fluorescent Assay 试剂盒分别检测细胞的凋亡及 Caspase-3活性。结果当 VK2浓度从10~(-7)mol/L 增加到10~(-4)mol/L 时,细胞生长抑制率由12.5%增加到59.7%(P<0.01)。VK2对细胞的黏附抑制能力呈剂量依赖关系(P<0.01);100μmol/L的 VK2作用细胞3 h 后,细胞对 Fibronectin 黏附抑制率为69.9%。作用48 h 后,细胞侵袭抑制率为65.5%(P<0.01);作用6 h 后,细胞凋亡率为(28.5±1.6)%,与此同时,细胞 Caspase-3活性为(226.0±6.4),与对照组(92.0±5.8)比较差异有统计学意义(P<0.01);预先加入 Caspase-3抑制剂(Z-VAD-FMK)后,Caspase-3活性无明显变化90.0±4.3(P>0.05)。结论 VK2对体外培养的 MHCC97H 细胞具有抑制生长、抑制黏附、抑制侵袭和诱导凋亡作用;Caspase-3参与了细胞凋亡的调控。
Objective To observe the effect of VK2 on the growth, adhesion, invasion, apoptosis and the activity of Caspase-3 in MHCC97H cells. Methods MTT assay was used to detect cell growth and cell adhesion and invasion in vitro. Cell apoptosis and Caspase-3 expression were detected by Annexin V-FITC Apoptosis Detection K and Caspase-3 Fluorescent Assay kit respectively. active. Results When the concentration of VK2 was increased from 10 -7 mol / L to 10 -4 mol / L, the cell growth inhibition rate increased from 12.5% to 59.7% (P <0.01). VK2 inhibited the adhesion of cells in a dose-dependent manner (P <0.01). The inhibition rate of VK2 cells treated with 100 μmol / L of VK2 for 3 h was 69.9%. After 48 h treatment, the cell invasion inhibition rate was 65.5% (P <0.01), and the apoptosis rate was (28.5 ± 1.6)% after 6 h treatment. Meanwhile, the activity of Caspase-3 was (226.0 ± 6.4) (P <0.01). Compared with the control group (92.0 ± 5.8), there was a significant difference (P <0.01). Caspase-3 activity did not change significantly after pretreatment with Caspase-3 inhibitor (90.0 ± 4.3, P> 0.05). Conclusion VK2 can inhibit the growth, inhibit the adhesion, inhibit the invasion and induce the apoptosis of MHCC97H cells cultured in vitro. Caspase-3 is involved in the regulation of apoptosis.