Xu Haiyang, Wang Jinghua, Zhang Jingjing, Li Mingxian
The First Hospital of Jilin University No. 71 Xinmin Street, Changchun 130021, Jilin, China.
Int J Clin Exp Pathol. 2017 Oct 1;10(10):10584-10592. eCollection 2017.
This study was designed to investigate the effect of TSG (2, 3, 5, 4'-tetrahydroxystibene-2-O-β-D-glucoside) on ischemic cardiomyopathy (ICM) related cell apoptosis and the mechanism related to it .
Rat cardiomyoblast cell line H9c2 was cultured in oxygen-glucose withdrawal medium for 8 hours to establish an cell model of oxygen-glucose deprivation (OGD). Cells were pretreated with TSG to test the protective effect of it against OGD. Cell viability, apoptosis, mitochondrial transmembrane potential (ΔΨ), and apoptosis related proteins were detected using appropriated methods. Differences between treatments were analyzed.
OGD treatment inhibited cell viability, expression of Akt and Bax, induced loss of ΔΨ, cell apoptosis, and triggered expression of Bcl-2 and Caspase-3/9. TSG pretreatment, on the contrary, suppressed OGD-induced cell apoptosis, ΔΨ loss, Bcl-2 and Caspase-3/9 expression, and promoted OGD-inhibited cell viability, Bax and Akt expression.
We concluded that TSG's protective effect against OGD-induced ischemic cell model was associated to Akt/Caspase-3 pathway. TSG might be explored as a therapeutic target for ICM.
本研究旨在探讨2,3,5,4'-四羟基二苯乙烯-2-O-β-D-葡萄糖苷（TSG）对缺血性心肌病（ICM）相关细胞凋亡的影响及其相关机制。
将大鼠心肌成纤维细胞系H9c2在无糖无血清培养基中培养8小时，建立氧糖剥夺（OGD）细胞模型。用TSG预处理细胞，以检测其对OGD的保护作用。采用适当方法检测细胞活力、凋亡、线粒体跨膜电位（ΔΨ）及凋亡相关蛋白。分析各处理组之间的差异。
OGD处理抑制细胞活力、Akt和Bax表达，诱导ΔΨ丧失、细胞凋亡，并引发Bcl-2和Caspase-3/9表达。相反，TSG预处理可抑制OGD诱导的细胞凋亡、ΔΨ丧失、Bcl-2和Caspase-3/9表达，并促进OGD抑制的细胞活力、Bax和Akt表达。
我们得出结论，TSG对OGD诱导的缺血细胞模型的保护作用与Akt/Caspase-3通路有关。TSG可能作为ICM的治疗靶点进行研究。
