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摘要：
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摘要：目的 探讨氧化苦参碱（oxymatrine，OMT）与HCV NS5A蛋白反式激活基因13（HCV NS5A
trans-regulated protein 13，NS5ATP13）的关系及对人肝母细胞瘤细胞系HepG2增殖凋亡的影响及其作
用机制。方法 在HepG2细胞中分别加入OMT、转染NS5ATP13过表达载体（pNS5ATP13）和小干扰
RNA（siNS5ATP13）及各自的阴性对照，检测细胞活力、愈合速度、迁移及侵袭程度、Caspase-3/7
表达水平及增殖凋亡相关蛋白的表达。结果 ①OMT能抑制HepG2细胞增殖，促进HepG2细胞凋亡，
下调NS5ATP13；②过表达NS5ATP13能促进HepG2细胞的增殖、迁移；干扰NS5ATP13能促进HepG2
细胞凋亡；③将NS5ATP13干扰后加入OMT能显著抑制细胞增殖、迁移，并抑制AKT/GSK/mTOR信
号转导通路。结论 OMT可能通过下调NS5ATP13抑制AKT/GSK/mTOR信号转导通路，诱导人肝母细
胞瘤HepG2细胞系的凋亡。
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Abstract: Objective To investigate the relationship between oxymatrine (OMT) and HCV NS5A trans-
regulated protein 13 (NS5ATP13) and their effects on proliferation and apoptosis of human hepatoblastoma
cell line HepG2. Methods OMT, NS5ATP13 overexpression vector (pNS5ATP13), small interfering RNA
(siNS5ATP13) and their respective negative controls were added to HepG2 cells, respectively, to detect the
changes in cell viability (CCK-8), healing rate (scratches), migration and invasion (invasion and migration
experiments), Caspase-3/7 expression levels, and expression of proliferation and apoptosis related genes.
Results ①OMT could inhibit the proliferation and promote the apoptosis of HepG2 cells, and also down-
regulate NS5ATP13 in HepG2 cells. ②Overxpression of NS5ATP13 could promote the proliferation and
migration of HepG2 cells; while NS5ATP13 silencing could promote the apoptosis of HepG2 cells. ③After
NS5ATP13 silencing, OMT could significantly modulate the proliferation, migration and AKT/GSK/mTOR
signaling pathway in HepG2 cells. Conclusion OMT may induce the apoptosis of human hepatoblastoma
HepG2 cell line by down-regulating NS5ATP13 and AKT/GSK/mTOR signaling pathway.
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