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目的:探讨中药单体淫羊藿苷(ICA)、黄芩苷(BAI)联合化疗药多柔比星(ADM)抑制肝癌HepG2细胞APRIL、VEGF的表达,进而抑制血管内皮细胞生长的作用机制。方法:MTT法检测血管内皮细胞ECV304的增殖活性;RT-PCR法检测HepG2细胞APRIL表达水平和ECV304细胞中APRIL受体HSPG的表达情况;免疫细胞化学检测HepG2细胞VEGF表达水平。结果:HepG2细胞中VEGF蛋白、APRIL和ECV304细胞中APRIL受体HSPG的mRNA均呈高表达状态,且APRIL与VEGF两者高表达呈显著正相关(P<0.001);HepG2细胞经25μg/mLICA、200μg/mLBAI、2μg/mLADM以及12.5μg/mLICA+1μg/mLADM、100μg/mLBAI+1μg/mLADM5组药物处理后,与未用药对照组相比,APRILmRNA表达水平明显下降;HepG2细胞经5组药物处理后的上清液与未用药对照组相比,对ECV304细胞具有明显的增殖抑制作用,抑制率分别为(2.79±5.57)%、(15.20±3.79)%、(12.10±4.50)%、(19.34±8.17)%和(20.27±4.77)%(P均<0.05);HepG2细胞经5组药物处理后,与未用药对照组相比,VEGF的表达水平明显下降。结论:A-PRIL具有促进静脉内皮细胞ECV304增殖的作用。ICA、BAI联合ADM能降低HepG2细胞中APRIL与VEGF的表达水平,从而发挥其抑制血管内皮细胞ECV304生长的作用。
Objective: To investigate the mechanism of ICA, BAI combined with chemotherapeutic drug adriamycin (ADM) inhibiting the expression of APRIL and VEGF in HepG2 cells and inhibiting the growth of vascular endothelial cells. Methods: The proliferation activity of ECV304 was detected by MTT assay. The expression of APRIL in HepG2 cells and the expression of HSPG receptor in ECV304 cells were detected by RT-PCR. The expression of VEGF in HepG2 cells was detected by immunocytochemistry. Results: The mRNA expression of APRIL and HSPG in HepG2 cells was significantly higher than that in APRIL and ECV304 cells (P <0.001). HepG2 cells were treated with 25 μg / mL of ICAO, APRIL mRNA expression was significantly decreased compared with untreated control group after 200μg / mLBAI, 2μg / mLADM and 12.5μg / mLICA + 1μg / mLADM, 100μg / mLBAI + 1μg / mLADM5group; HepG2cells were treated with5groups of drugs Compared with the control group, ECV304 cells had a significant inhibitory rate of (2.79 ± 5.57)%, (15.20 ± 3.79)%, (12.10 ± 4.50)%, (19.34 ± 8.17)% and (20.27 ± 4.77)%, respectively (all P <0.05). Compared with the untreated control group, the expression of VEGF in HepG2 cells treated with 5 groups of drugs decreased significantly. Conclusion: A-PRIL can promote the proliferation of ECV304 cells. ICA and BAI combined with ADM can decrease the expression of APRIL and VEGF in HepG2 cells and thus exert their inhibitory effect on the growth of ECV304 in vascular endothelial cells.