Yang Liu, Wang Yeqiu, An Lifeng, Zhang Xinya, Wang Jing, Wang Yi, Cheng Ruyang, Li Chenxiang, Ma Wei
College of Jiamusi, Heilongjiang University of Chinese Medicine, Jiamusi, Heilongjiang 154007, China.
College of Pharmacy, Heilongjiang University of Chinese Medicine, Harbin, Heilongjiang 150040, China.
Appl Bionics Biomech. 2022 May 11;2022:6113352. doi: 10.1155/2022/6113352. eCollection 2022.
In recent years, the incidence of depression is on the rise. Our paper proposed to study the protective effects of Schisandrin on CORT-induced PC12 depressive cell model and the underlying mechanisms.
The in vitro models of PC12 were established using corticosterone (CORT). 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) method was used to screen the effective concentration of Schisandrin, and the models of PC12 were treated with low, medium, and high concentrations of Schisandrin. The cell activity of each group was detected by MTT assay. The LDH activity in each group of cells was detected by lactate dehydrogenase (LDH) kit. Apoptosis rate of each group was detected by Annexin V-FITC apoptosis assay kit. Mitochondrial membrane potential of each group of cells was detected by mitochondrial membrane potential kit. The protein expression levels of Caspase-3, Bax, and Bcl-2 in each group of cells were detected by western blot.
The treatment of Schisandrin significantly increased the cell viability in models of PC12. In addition, the results of LDH activity suggested that Schisandrin significantly reduced LDH content in models of PC12. Consistently, Schisandrin reduced the mitochondrial membrane potential of CORT-induced PC12 depressive cell model. Furthermore, Schisandrin effectively reduced the number of apoptotic cells and inhibited the expression of proapoptotic-related proteins (cleaved Caspase-3 and Bax) but increased the antiapoptotic-related protein (Bcl-2) in the models of PC12.
Protective effects of Schisandrin on CORT-induced PC12 depressive cell model by inhibiting cells apoptosis in vitro.
近年来，抑郁症的发病率呈上升趋势。我们的论文旨在研究五味子醇对皮质酮诱导的PC12抑郁细胞模型的保护作用及其潜在机制。
用皮质酮（CORT）建立PC12体外模型。采用3-(4,5-二甲基噻唑-2-基)-2,5-二苯基四氮唑溴盐（MTT）法筛选五味子醇的有效浓度，并用低、中、高浓度的五味子醇处理PC12模型。通过MTT法检测每组细胞的活性。用乳酸脱氢酶（LDH）试剂盒检测每组细胞中的LDH活性。用膜联蛋白V-异硫氰酸荧光素（Annexin V-FITC）凋亡检测试剂盒检测每组的凋亡率。用线粒体膜电位试剂盒检测每组细胞的线粒体膜电位。通过蛋白质免疫印迹法检测每组细胞中半胱天冬酶-3（Caspase-3）、促凋亡蛋白（Bax）和抗凋亡蛋白（Bcl-2）的蛋白表达水平。
五味子醇处理显著提高了PC12模型中的细胞活力。此外，LDH活性结果表明，五味子醇显著降低了PC12模型中的LDH含量。同样，五味子醇降低了皮质酮诱导的PC12抑郁细胞模型的线粒体膜电位。此外，五味子醇有效减少了凋亡细胞的数量，抑制了促凋亡相关蛋白（裂解的Caspase-3和Bax）的表达，但增加了PC12模型中抗凋亡相关蛋白（Bcl-2）的表达。
五味子醇通过在体外抑制细胞凋亡对皮质酮诱导的PC12抑郁细胞模型具有保护作用。
