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摘要：
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摘要：目的 探讨人参皂苷Rh2（ginsenoside Rh2，G-Rh2）与三氧化二砷反式激活蛋白3（arsenic-
transactivated protein 3，AsTP3）间的关系及其对HepG2细胞糖代谢的影响和作用机制。方法 将
G-Rh2、AsTP3基因的过表达载体（pAsTP3）、小干扰RNA（siAsTP3）及其各自的阴性对照分别
作用于HepG2细胞，通过检测细胞内葡萄糖水平、ROS水平及糖代谢相关基因的表达探讨G-Rh2
与AsTP3的关系以及对HepG2细胞糖代谢的影响。结果 ①G-Rh2可降低HepG2细胞内葡萄糖和
ROS水平，并下调叉头转录因子1（forkhead box protein O1，FoxO1）的表达、上调磷酸化蛋白激
酶B（phosphoprotein kinase B，p-PKB，又称p-AKT）的表达，从而使磷酸烯醇式丙酮酸羧激酶1
（PEPCK1）mRNA和蛋白表达水平上升，6-磷酸葡萄糖脱氢酶（G6PD） mRNA和蛋白表达水平下
降；②与G-Rh2类似，过表达AsTP3后HepG2细胞内葡萄糖和ROS水平降低，FoxO1蛋白表达下降，
p-AKT蛋白表达上升，PEPCK1 mRNA表达上升，G6PD mRNA表达下降，而干扰AsTP3表达后结果则
相反；③G-Rh2可上调AsTP3基因表达，在干扰AsTP3表达的情况下加用G-Rh2，其促进肝葡萄糖产生
的作用减弱。结论 G-Rh2具有减少肝脏糖异生的作用，其机制可能是通过调控AsTP3及p-AKT/FoxO1
信号转导通路调节肝脏糖代谢相关基因的表达而实现。
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Abstract: Objective To investigate the relationship between ginsenoside Rh2 (G-Rh2) and arsenic-
transactivated protein 3 (AsTP3), and its effects and mechanisms on the glucose metabolism of HepG2
cells. Methods G-Rh2, AsTP3 overexpression vector (pAsTP3), small interfering RNA (siAsTP3) and
their respective negative controls were applied to HepG2 cells, respectively. Glucose level, ROS level and
the expression of genes related to glucose metabolism were detected to explore the relationship between
G-Rh2 and AsTP3 and its effects on glucose metabolism of HepG2 cells. Results ①G-Rh2 could decrease
the levels of glucose and ROS in HepG2 cells, down-regulate the expression level of Forkhead box protein
O1 (FoxO1) and up-regulate the expression level of phosphoprotein kinase B (p-AKT), so as to increase
the expression levels of phosphoenolpyruvate carboxykinase 1 (PEPCK1) mRNA and protein, and decrease
the expression levels of 6-phosphoglucose dehydrogenase (G6PD) mRNA and protein. ②Similar to G-Rh2,
after overexpression of AsTP3, the levels of glucose, ROS and FoxO1 protein in HepG2 cells decreased,
the expressions of p-AKT protein and PEPCK1 mRNA increased, and the expression of G6PD mRNA
decreased, while the results were reversed after interference of AsTP3 expression. ③G-Rh2 could up-regulate
the expression of AsTP3 gene. In the case of interfering with the expression of AsTP3, the effects of G-Rh2
on promoting hepatic glucose production was weakened. Conclusions G-Rh2 can reduce the regulation of
hepatic gluconeogenesis, which may be achieved by regulating AsTP3 and p-AKT/FoxO1 signaling pathway
to regulate the expression of glucose metabolism related genes in the liver.
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