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摘要
起的细胞凋亡作用,C20 和C40 抵抗PA 诱导的心肌凋亡可能与炎症信号通路相
关。
结论:1)绿原酸类似物CGA-6 抵抗H O 诱导的H9c2 心肌细胞损伤作用优
2 2
于绿原酸,其可能的机制是经其抗氧化应激参与的线粒体凋亡通路途径和抑制
JNK 及ERK 的激活减少细胞凋亡;2 )获得4 个抵抗PA 诱导H9c2 心肌细胞脂
毒性损伤活性强于姜黄素的衍生物。
关键词: 氧化应激;心肌细胞凋亡;天然产物;线粒体;MAPK ;脂毒性
Abstract
Abstract
Objects: To obtain natural compounds or highly effective derivatives/analogues
that protected cardiomyocytes from oxidative stress or lipotoxicity, and investigate
their anti-apoptotic mechanisms.
Methods: 1) H9c2 cells were treated with H O at different concentrations, cell
2 2
viability was tested by MTT to determine the most appropriate experiment
concentration. 2) H9c2 cells were divided into 4 groups according to different
treatments (control group, CGA-6 group, H O group, H O +CGA-6 group), cell
2 2 2 2
viability was assayed with MTT. The lactate dehydrogenase (LDH) release and
catalase (CAT) activity measurement were performed according to kit protocols. The
intracellular reactive oxygen species, Ca2+, mitochondrial membrane potential (MMP),
were measured with CM-H DCFDA, Fluo-4 and JC-1 fluorescent probes,
2
respectively; The DNA was stained with Hoechst 33342 to observe cell apoptosis;
Expression level of proteins related to mitochondrial apoptotic pathways and MAPKs
were analyzed by western blot. 3) Time and dose-dependent palmitate-induced H9c2
cells viability were tested by MTT and the most appropriate experiment
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