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目的:探讨重组人P53腺病毒(recombinant human adenovirus-P53,rAd-P53)联合紫杉醇对宫颈癌HeLa细胞增殖、凋亡及血管内皮生长因子(vascular endothelial growth factor,VEGF)表达的影响。方法:MTT法检测紫杉醇、rAd-P53单独或联合应用后HeLa细胞的增殖;DAPI染色法检测紫杉醇、rAd-P53单独或联合作用48 h后HeLa细胞的凋亡;Western blotting法检测紫杉醇、rAd-P53单独或联合作用后HeLa细胞VEGF的表达情况。结果:紫杉醇、rAd-P53单独或联合作用24～72 h均能抑制HeLa细胞的增殖,抑制作用具有时效和量效关系,且联合用药组对HeLa细胞的抑制率显著高于单用紫杉醇组及rAd-P53组(P<0.05);联合作用时的相互作用系数(coefficient of drug interaction,CDI)均<1,说明两者具有协同作用;rAd-P53(5×107VP/ml)联合紫杉醇(3μg/ml)作用48 h后,对HeLa细胞增殖的抑制率高于两药单用组[(54.0±0.92)%vs(31.8±0.58)%、(27.2±0.55)%,P<0.05]。联合用药组HeLa细胞的凋亡率也显著高于紫杉醇组、rAd-P53单用组[(83±0.07)%vs(36±0.04)%、(62±0.05)%,P<0.05]。联合用药组HeLa细胞中VEGF的表达显著低于两单独用药组,HeLa细胞中VEGF表达分别下降(81±0.08)%、(45±0.07)%和(60±0.06)%(P<0.05)。结论:rAd-P53和紫杉醇联合用药抑制HeLa细胞的增殖、诱导细胞凋亡的效果优于单独用药,其机制可能与下调VEGF表达有关。
Objective: To investigate the effects of recombinant human adenovirus-P53 (rAd-P53) and paclitaxel on the proliferation, apoptosis and the expression of vascular endothelial growth factor (VEGF) in cervical cancer HeLa cells. Methods: MTT assay was used to detect the proliferation of HeLa cells treated with paclitaxel and rAd-P53 alone or in combination. The apoptosis of HeLa cells treated with paclitaxel and rAd-P53 alone or in combination for 48 h was detected by DAPI staining. The paclitaxel, rAd- The expression of VEGF in HeLa cells treated with P53 alone or in combination. Results: Paclitaxel and rAd-P53 could inhibit the proliferation of HeLa cells either alone or in combination for 24-72 h. The inhibitory effect of paclitaxel and rAd-P53 on HeLa cells was significantly higher than that of paclitaxel alone or in combination group P53 (5μg / ml) and rAd-P53 group (P <0.05). Coefficients of drug interaction (CDI) / ml) for 48 h, the inhibitory rate of HeLa cell proliferation was higher than that of the two drugs alone group (54.0 ± 0.92)% vs (31.8 ± 0.58)%, (27.2 ± 0.55)%, P <0.05. The apoptotic rate of HeLa cells in the combination group was also significantly higher than that in the paclitaxel group (83 ± 0.07 vs 36 ± 0.04, 62 ± 0.05, P <0.05, respectively). The expression of VEGF in HeLa cells in combination group was significantly lower than that in HeLa cells alone (81 ± 0.08), (45 ± 0.07)% and (60 ± 0.06)%, respectively (P <0.05). Conclusion: The combination of rAd-P53 and paclitaxel can inhibit the proliferation of HeLa cells and induce the apoptosis of HeLa cells. The mechanism of the combination of rAd-P53 and paclitaxel may be related to the down-regulation of VEGF expression.