Toll样受体4特异性拮抗剂TAK-242对人卵巢癌细胞株SKOV-3增殖、凋亡的影响及其机制

发布时间：2019-04-26 20:17

【摘要】：目的观察Toll样受体4(TLR4)特异性拮抗剂TAK-242对人卵巢癌细胞株SKOV-3增殖、凋亡的影响,并探讨其可能作用机制。方法取对数生长期人卵巢癌SKOV-3细胞分为A组、B组、对照组及空白组,A、B组分别加入终浓度为20、40 nmol/L的TAK-242培养,对照组加入1%DMSO,空白组不做任何处理。采用MTT比色法观察给药24、48、72 h时各组细胞增殖情况,采用Annexin-V/PI观察给药24、48、72 h时各组凋亡细胞。采用Western blotting法检测给药48 h时各组细胞核因子-κB(NF-κB)p65、总蛋白细胞周期蛋白D1(CyclinD1)、裂解的半胱氨酸天冬氨酸特异性蛋白酶-3(cleaved-caspse 3)。结果给药24、48、72 h时,A、B组细胞增殖抑制率均高于对照组、空白组(P均0.05);给药24、48、72 h时,B组细胞增殖抑制率均高于A组(P均0.05);随给药时间延长,B组细胞增值抑制率升高(P均0.05)。给药24、48、72 h时,A、B组细胞凋亡率均高于对照组、空白组(P均0.05);TAK-242浓度升高,细胞凋亡率升高,随给药时间延长,细胞凋亡率升高(P均0.05);随给药时间增加,B组细胞增值抑制率升高(P均0.05)。给药48 h时,细胞NF-κB p65、CyclinD1蛋白相对表达量低于空白组和对照组,cleaved-caspase 3相对表达量高于空白组和对照组(P均0.05)。结论 TAK-242可抑制人卵巢癌细胞的增殖、促进细胞凋亡,其机制可能为NF-κB信号通路功能被抑制。
[Abstract]:Aim to observe the effect of Toll-like receptor 4 (TLR4) specific antagonist TAK-242 on proliferation and apoptosis of human ovarian cancer cell line SKOV-3 and explore its possible mechanism. Methods Human ovarian cancer SKOV-3 cells in logarithmic growth stage were divided into three groups: group A, group B, control group and blank group, group A and group B were cultured with TAK-242 with final concentration of 20,40 nmol/L respectively, and control group were added with 1% DMSO. No treatment was done in the blank group. MTT colorimetry was used to observe the proliferation of the cells at 24,48,72 h, and Annexin-V/PI was used to observe the apoptotic cells at 24,48 and 72 h. Nuclear factor-魏 B (NF- 魏 B) p65, total protein cyclin D1 (CyclinD1) and lysed caspase-3 (cleaved-caspse-3) were detected by Western blotting assay at 48 h after administration. Results the inhibitory rate of cell proliferation in group A and B was higher than that in control group (P 0.05) at 24,48,72 h, and the inhibition rate of cell proliferation in group B was higher than that in group A at 24,48 and 72 h (all P 0.05), and that in group B was higher than that in group A at 24,48 and 72 h (all P 0.05). With the prolongation of the administration time, the inhibition rate of cell proliferation in group B increased (all P 0.05). At 24,48,72 h after administration, the apoptosis rate in group A and B was higher than that in control group and blank group (P0.05), and the apoptosis rate increased with the increase of TAK-242 concentration, and increased with the prolongation of administration time (all P0.05), and the apoptosis rate in group A and B was significantly higher than that in control group (P < 0.05). With the increase of the time of administration, the inhibition rate of cell proliferation in group B increased (all P 0.05). After 48 h administration, the relative expression of NF- 魏 B p65, CyclinD1 protein was lower than that of blank group and control group, and the relative expression of cleaved-caspase 3 was higher than that of blank group and control group (P0.05). Conclusion TAK-242 can inhibit the proliferation of human ovarian cancer cells and promote the apoptosis of human ovarian cancer cells. The mechanism may be that the NF- 魏 B signaling pathway is inhibited.
【作者单位】：平顶山学院医学院;平顶山市第一人民医院;
【分类号】：R737.31

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