Li Xin, Zhang Hong-mei, Niu Qiao, Yuan Fu-sheng
Department of Radiation Health, Control of Disease Control of Taiyuan Iron Steel Company, Taiyuan 030003, China.
Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi. 2012 Feb;30(2):85-8.
To study the expression levels of cdk5, p35 and p53 genes in arsenic trioxide (As2O3O)-induced neuron apoptosis and to explore the potential mechanism.
The cultured primary rats' neurons were divided into 5 groups, which were exposed to 0, 1, 5, 10 micromol/L As2O3 and dimethyl sulfoxide (DMSO) for 8 h, respectively. The cell viability and cell apoptosis were detected by MTT colouration methods and flow cytometry, respectively. The real-time fluorescence quantitative PCR was used to measured the expression levels of cdk5, p35 and p53 genes.
The cell viability inhibition rates were 16.77%, 19.72% and 27.81% in 1, 5, 10 micromol/L As203 groups, respectively. Compared to the untreated group and DMSO group, the cell apoptosis rates were significantly increased in 5 and 10 micromol/L As2O3 groups (P < 0.05). The expression levels of cdk5, p35 and p53 genes increased with the exposure doses of AsO3. However, there were no significant differences in p35 gene expression between different dose subgroups (P > 0.05). There were significant differences in cdk5 and p53 gene expression between different dose subgroups (P < 0.05). The expression levels of cdk5 gene in 5 and 10 micromol/L As2O3 groups were significantly higher than those in untreated group and DMSO group (P < 0.05). The expression levels of p53 gene in 1, 5 and 10 micromol/L As2O3 groups were significantly higher than that in untreated group (P < 0.05). The expression level of p53 gene in 10 mciromol/L As2O3 group was significantly higher than that in DMSO group (P < 0.05).
Cdk5, p35 and p53 genes may involve in the process of As2O3-induced neural cell apoptosis.
研究三氧化二砷(As₂O₃)诱导神经元凋亡过程中细胞周期蛋白依赖性激酶5(cdk5)、p35和p53基因的表达水平,并探讨其潜在机制。
将培养的原代大鼠神经元分为5组,分别用0、1、5、10 μmol/L三氧化二砷和二甲基亚砜(DMSO)处理8小时。分别采用MTT比色法和流式细胞术检测细胞活力和细胞凋亡情况。采用实时荧光定量PCR检测cdk5、p35和p53基因的表达水平。
1、5、10 μmol/L As₂O₃组细胞活力抑制率分别为16.77%、19.72%和27.81%。与未处理组和DMSO组相比,5和10 μmol/L As₂O₃组细胞凋亡率显著升高(P < 0.05)。cdk5、p35和p53基因的表达水平随As₂O₃暴露剂量的增加而升高。然而,不同剂量亚组间p35基因表达无显著差异(P > 0.05)。不同剂量亚组间cdk5和p53基因表达有显著差异(P < 0.05)。5和10 μmol/L As₂O₃组cdk5基因表达水平显著高于未处理组和DMSO组(P < 0.05)。1、5和10 μmol/L As₂O₃组p53基因表达水平显著高于未处理组(P < 0.05)。10 μmol/L As₂O₃组p53基因表达水平显著高于DMSO组(P < 0.05)。
Cdk5、p35和p53基因可能参与了As₂O₃诱导神经细胞凋亡的过程。