大黄素甲醚对皮质酮损伤PC12细胞保护作用研究
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摘要
目的观察大黄素甲醚对皮质酮损伤PC12细胞的影响。方法体外培养PC12细胞,皮质酮处理后给予大黄素甲醚干预。采用CCK-8法检测皮质酮毒性及大黄素甲醚作用于皮质酮损伤后PC12细胞存活率;流式细胞仪检测PC12细胞凋亡;氮蓝四唑还原法检测PC12细胞内活性氧(ROS)水平;Western blot测定PC12细胞内脑源性神经营养因子(BDNF)蛋白表达。结果与空白组比较,模型组PC12细胞活力明显降低(P<0.01);与模型组比较,大黄素甲醚组PC12细胞活力增强,PC12细胞凋亡率降低,PC12细胞内ROS含量降低,PC12细胞内BDNF蛋白表达升高。结论大黄素甲醚对皮质酮诱导的PC12细胞损伤具有保护作用。
Objective To observe the effects of physcion on PC12 cells injured by corticosterone. Methods PC12 cells were cultured in vitro, and the cells were treated with physcion after corticosterone intervention. CCK-8 was used to detect corticosterone toxicity and the survival rate of PC12 cells injured by corticosterone after treated by physcion. The apoptosis of PC12 cells was detected by flow cytometry. The level of intracellular ROS was determined by NBT reduction assay. BDNF protein expression in PC12 cells was detected by Western blot. Results Compared with the blank group, the viability of PC12 cells in the model group decreased(P<0.01); Compared with the model group, the viability of PC12 cells increased, apoptosis rate of PC12 cells decreased, ROS content in PC12 cells decreased, and BDNF protein expression in PC12 cells increased in the physcion group. Conclusion Physcion has protective effects on corticosterone-induced PC12 cellular damage.
Objective To observe the effects of physcion on PC12 cells injured by corticosterone. Methods PC12 cells were cultured in vitro, and the cells were treated with physcion after corticosterone intervention. CCK-8 was used to detect corticosterone toxicity and the survival rate of PC12 cells injured by corticosterone after treated by physcion. The apoptosis of PC12 cells was detected by flow cytometry. The level of intracellular ROS was determined by NBT reduction assay. BDNF protein expression in PC12 cells was detected by Western blot. Results Compared with the blank group, the viability of PC12 cells in the model group decreased(P<0.01); Compared with the model group, the viability of PC12 cells increased, apoptosis rate of PC12 cells decreased, ROS content in PC12 cells decreased, and BDNF protein expression in PC12 cells increased in the physcion group. Conclusion Physcion has protective effects on corticosterone-induced PC12 cellular damage.
引文
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[13]MOLTENI R,CALABRESE F,CHOURBAJI S,et al.Depression-prone mice with reduced glucocorticoid receptor expression display an altered stress-dependent regulation of brain-derived neurotrophic factor and activity-regulated cytoskeleton-associated protein[J].Journal of Psychopharmacology,2010,24(4):595-603.
[14]CHEN H,LOMBèS M,LE M D.Glucocorticoid receptor represses brain-derived neurotrophic factor expression in neuron-like cells[J].Molecular Brain,2017,10(1):12.
[2]童妍,郝安辉,李坤伦,等.大黄素甲醚对抑郁大鼠海马ERK、c AMP、Ca MK的影响[J].中药药理与临床,2016,32(2):73-76.
[3]熊兴富.中药大黄主要有效成分药理学研究进展[J].中医临床研究,2014,6(10):143-146.
[4]蔡可而,王严飞,陆豫.大黄素甲醚衍生物的合成及抗肿瘤活性的研究[J].化学试剂,2014,36(4):313-314,377.
[5]荔志云,张明,季玮,等.大黄素甲醚对PC12细胞缺氧损伤的保护作用[J].中国临床神经外科杂志,2013,18(12):738-741.
[6]童妍,金钊,赵焕瑛.大黄素甲醚对慢性轻度不可预见应激大鼠海马单胺类神经递质的影响[J].中药药理与临床,2015,31(1):54-57.
[7]KUNUGI H,HORI H,NUMAKAWA T,et al.The hypothalamic-pituitaryadrenal axis and depressive disorder:recent progress[J].Japanese Journal of Psychopharmacology,2012,32(4):203.
[8]KASCKOW J W,BAKER D,JR G T.Corticotropin-releasing hormone in depression and post-traumatic stress disorder[J].Peptides,2001,22(5):845-851.
[9]JOKINEN J,NORDSTR?M P.HPA axis hyperactivity and attempted suicide in young adult mood disorder inpatients[J].Journal of Affective Disorders,2009,116(2):117-120.
[10]XIONG Y,REN L,WANG Z,et al.Anti-proliferative effect of Physcion on human gastric cell line via inducing ROS-dependent apoptosis[J].Cell Biochemistry&Biophysics,2015,73(2):537.
[11]KURITA M,NISHINO S,KATO M,et al.Plasma brain-derived neurotrophic factor levels predict the clinical outcome of depression treatment in a naturalistic study[J].PLo S One,2012,7(6):e39212.
[12]李晓照,陈泽奇,胡随瑜,等.抑郁症患者血清BDNF水平与相关因素分析[J].中国临床心理学杂志,2005,13(3):312-313.
[13]MOLTENI R,CALABRESE F,CHOURBAJI S,et al.Depression-prone mice with reduced glucocorticoid receptor expression display an altered stress-dependent regulation of brain-derived neurotrophic factor and activity-regulated cytoskeleton-associated protein[J].Journal of Psychopharmacology,2010,24(4):595-603.
[14]CHEN H,LOMBèS M,LE M D.Glucocorticoid receptor represses brain-derived neurotrophic factor expression in neuron-like cells[J].Molecular Brain,2017,10(1):12.