Abstract

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.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.