Zeng Jianwei, Chen Shiqiang, Li Na, Chen Liang, Su Jiaosu, Niu Guangjun, Zhu Si, Liang Yichi
Academy of Integrative Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian 350122, P.R. China.
College of Pharmacy, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian 350122, P.R. China.
Mol Med Rep. 2015 Aug;12(2):1997-2002. doi: 10.3892/mmr.2015.3666. Epub 2015 Apr 23.
The present study aimed to elucidate the molecular mechanisms underlying the induction of cytotoxic effects by sasanquasaponin (SQS) in HepG2 cells. Following SQS treatment, time- and dose-dependent increases in the apoptotic rate were observed. The induction of cell death by SQS mainly occurs via programmed cell death, as indicated by Annexin V-fluorescein isothiocyanate and propidium iodide staining, where up to 30% apoptotic cells were detected following 12 h SQS treatment. Reverse transcription-polymerase chain reaction analysis demonstrated that SQS treatment upregulated B-cell lymphoma-2 (Bcl-2)-associated x protein and caspase-3 mRNA expression and downregulated Bcl-2 mRNA expression. Greater alterations in Bax, Bcl-2 and caspase-3 expression were observed with increasing treatment duration. The decrease in Bcl-2, increase in Bax and, finally, the activation of caspase-3 in HepG2 cells indicated that the apoptotic process induced by SQS was irreversible. The results of the present study therefore suggested that SQS induced HepG2 cell apoptosis via the activation of mitochondrial apoptotic pathways.
本研究旨在阐明山茶花皂苷（SQS）诱导HepG2细胞产生细胞毒性作用的分子机制。SQS处理后，观察到凋亡率呈时间和剂量依赖性增加。SQS诱导的细胞死亡主要通过程序性细胞死亡发生，膜联蛋白V-异硫氰酸荧光素和碘化丙啶染色表明，SQS处理12小时后检测到高达30%的凋亡细胞。逆转录-聚合酶链反应分析表明，SQS处理上调了B细胞淋巴瘤-2（Bcl-2）相关X蛋白和半胱天冬酶-3 mRNA表达，并下调了Bcl-2 mRNA表达。随着处理时间的延长，Bax、Bcl-2和半胱天冬酶-3表达的变化更大。HepG2细胞中Bcl-2的减少、Bax的增加以及最终半胱天冬酶-3的激活表明，SQS诱导的凋亡过程是不可逆的。因此，本研究结果表明，SQS通过激活线粒体凋亡途径诱导HepG2细胞凋亡。
