南方医科大学学报

南方医科大学学报 ›› 2014, Vol. 34 ›› Issue (06): 832-.

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内质网应激途径在鬼臼毒素纳米脂质载体诱导VK2/E6E7细胞凋亡的机制

王琦，韩凯，李雪芽，肖艳，曾抗   

  • 出版日期:2014-06-20 发布日期:2014-06-20

Role of endoplasmic reticulum stress pathway in podophyllotoxin nanostructured lipid
carriers-induced apoptosis of VK2/E6E7 cells

  • Online:2014-06-20 Published:2014-06-20

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摘要： 目的探讨鬼臼毒素纳米脂质载体（POD-NLC）通过内质网应激途径诱导体外永生化人阴道上皮细胞（VK2/E6E7 细
胞）凋亡的机制。方法自制0.5% POD-NLC和单纯-NLC，实验分为单纯-NLC、0.125 μg/mlPOD-NLC、0.25 μg/ml POD-NLC、
0.5 μg/ml POD-NLC和空白对照组，分别作用VK2/E6E7细胞24 h。采用激光扫描共聚焦显微镜（LSCM）检测各组细胞内Ca2+
浓度的变化；RT-PCR和Western blot法检测各组GRP78、GRP94和calpain2基因mRNA和蛋白表达。结果与空白对照组相比，
不同浓度POD-NLC 可呈浓度依赖性的增加细胞内Ca2 +浓度（P<0.01），各药物处理组之间比较有统计学差异（P<0.05）。
POD-NLC 可上调GRP78、GRP94、calpain2 基因mRNA和蛋白表达。单纯-NLC 和空白对照组之间差异无统计学意义（P>
0.05）。结论POD-NLC诱导VK2/E6E7细胞凋亡的分子机制可能与内质网应激反应性凋亡途径的启动有关。

Abstract: Objective To explore the mechanism of podophyllotoxin nanostructured lipid carriers (POD-NLC)-induced
apoptosis of VK2/E6E7 cells mediated by endoplasmic reticulum stress (ERS). Methods VK2/E6E7 cells cultured in vitro were
exposed to 0.125, 0.25, and 0.5 μg/ml POD-NLC or blank NLC for 24 h. The intracellular calcium concentration was measured
by laser scanning confocal microscopy (LSCM), and the expression levels of GRP78, GRP94, and calpain2 mRNA and proteins
in the cells were detected using RT-PCR and Western blotting. Results Compared with the control cells, the cells exposed to
POD-NLC showed a concentration-dependent increase of intracellular calcium concentration (P<0.01), and the differences
were statistically significant between different dose groups (P<0.05). RT-PCR and Western blotting showed that POD-NLC
up-regulated GRP78, GRP94 and calpain2 mRNA and proteins expressions, whish showed significant differences between
blank-NLC and the control groups (P>0.05). Conclusion POD-NLC induces apoptosis of VK2/E6E7 cells possibly by triggering
the endoplasmic reticulum stress response.