Document Type : Research articles

Authors

1 1Ji'an Key Laboratory of Biomedicine, College of Medicine, Jinggangshan University, Ji'an City, Jiangxi Province, China

2 2College of Medicine, Jiamusi University, Jiamusi City, Heilongjiang Province, China

3 Department of Human Anatomy, Histology and Embryology, College of Medicine, Jinggangshan University, Ji'an City, Jiangxi Province, China

Abstract

Background: Current studies have demonstrated the anti-cancer effects of paeonol in some tumors; however, its effect on gliomas remains unknown.
Objectives: This study aimed to investigate the anti-tumor effect of paeonol in human glioma tissues and cells including its effect and connection with apoptosis and oxidative stress in gliomas.
Methods: Cell Counting Kit-8 (CCK-8) was used to detect the antiproliferative effect of paeonol in human U251 glioma cells. Transwell and colony-forming assays were employed to assess the effect of paeonol on the ability of invasion and colony formation of U251 cells. Superoxide dismutase (SOD) activity, malondialdehyde (MDA) content, total antioxidant capacity (T-AOC), and catalase activity (CAT) were measured to evaluate the effect of paeonol on oxidative stress in U251 cells. Quantitative real-time polymerase chain reaction (RT-q) PCR and western blot were utilized to detect caspase-3 expression levels. Terminal deoxynucleotidyl transferase dUTP nick end-labeling (TUNEL) staining detected the effect of paeonol on U251 cell apoptosis.
Results: Paeonol decreased cell viability, as well as the proliferation, invasion, and colony formation ability of U251 cells. Paeonol reduced MDA content and increased the activities of SOD, CAT, and T-AOC in U251 cells. Caspase-3 expression was lower in human glioma tissues than in normal tissues of the human brain. Paeonol promoted U251 cell apoptosis as revealed by TUNEL staining results and the significant up-regulation of caspase-3 expression in U251 cells.
Conclusion: These results indicated that paeonol has anti-tumor and pro-apoptotic effects in gliomas via oxidative stress regulation and the caspase-3 pathway. Our study, therefore, provides new ideas for the clinical treatment of gliomas.

Keywords

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