复方柴归方对CORT诱导的低分化PC12抑郁细胞模型的保护作用及机制研究

Protective Effect and Mechanism of Compound Chaigui Decoction on CORT-Induced Poorly Differentiated PC12 Depression Cell Model

目的探讨复方柴归方(逍遥散化裁方,FFCGF)对皮质酮诱导的低分化PC12抑郁细胞模型的保护作用及其相关机制。方法采用皮质酮(CORT)诱导低分化PC12抑郁细胞模型,给予不同浓度(50、100、200μg·mL^(-1))FFCGF预处理PC12细胞36 h,MTT检测细胞活力,观察FFCGF对CORT(500μM)细胞损伤后的保护作用;检测细胞培养上清液中的LDH活性,判断药物对细胞膜的保护作用;使用Annexin VFITC/PI双染色法检测药物对CORT诱导的PC12细胞凋亡的保护作用;检测线粒体膜电位以及细胞内钙离子含量,观察FFCGF的保护作用。结果研究表明皮质酮诱导PC12细胞损伤以后,细胞的活力的指标下降,而乳酸脱氢酶释放率、细胞凋亡率及钙离子浓度指标升高。给予FFCGF后对应的指标发生回调,表明FFCGF对CORT诱导低分化PC12细胞损伤具有较好的保护作用。结论FFCGF对CORT诱导的低分化PC12抑郁细胞模型具有较好的保护作用。

Objective To explore the protective effect of the compound Chaigui Decoction(FFCGF) on corticosteroneinduced poorly differentiated PC12 depression cell model and its related mechanisms. Methods Corticosterone(CORT)was used to induce depression in PC12 depression cell model, PC12 cells were pretreated with FFCGF at different concentrations(50, 100, 200 μg·mL^(-1)) for 36 h. Cell viability was measured by MTT to observe the protective effect of FFCGF on CORT(500 μM) cells after injury;LDH activity in cell culture supernatant was measured The protective effect of FFCGF on CORT-induced apoptosis of PC12 cells was detected by using Annexin V-FITC/PI double staining;the mitochondrial membrane potential and intracellular calcium ion content were detected to observe the protective effect of FFCGF. Results It was shown that after corticosterone-induced PC12 cell injury, the indicators of cell viability decreased, while the indicators of lactate dehydrogenase release rate, apoptosis rate and calcium ion concentration increased. The corresponding indexes were regressed after the administration of FFCGF, indicating that FFCGF has a better protective effect on CORT-induced poorly differentiated PC12 cell injury. Conclusion FFCGF has a protective effect on CORT-induced poorly differentiated PC12 depressed cell model.Conclusion Compound Chaigui Decoction can protect CORT-induced poorly differentiated PC12 cell.