Effects of Coptidis Rhizoma on Cell Cycle, DNA Damage, and Apoptosis in L929 Murine Fibroblast Cells

• Published in: Chinese herbal medicines Vol. 8; no. 3; pp. 242 - 250
• Main Authors: Huang, Yan-fei, Gu, Man-man, Xu, Jing, Han, Chun-yang, Liu, Teng-fei, Liu, Cui-yan
• Format: Journal Article
• Language: English
• Published: Elsevier B.V 01.07.2016
• Subjects: apoptosis; cell cycle; Coptidis Rhizoma; cytotoxicity; DNA damage; DNA损伤; mitochondrial membrane potential; 小鼠; 成纤维细胞; 线粒体膜电位; 细胞凋亡; 细胞周期阻滞; 细胞存活率; 黄连; apoptosis; cell cycle; Coptidis Rhizoma; DNA damage; cytotoxicity; mitochondrial membrane potential
• ISSN: 1674-6384; 2589-3610
• DOI: 10.1016/S1674-6384(16)60046-1

Objective Coptidis Rhizoma （CR）, a widely used traditional Chinese herbal medicine, is commonly believed to be non-toxic. However, little is known about its cytotoxicity and relevant mechanisms at cellular and genetic levels. The present study was conducted to explore the cytotoxicity of CR and its mechanisms related to cell cycle arrest, DNA damage, cell apoptosis, and mitochondrial membrane potential in L929 murine fibroblast cells. Methods The cells were cultured and treated with different concentration of CR aqueous extract for 24 h. Cell viability was determined by CCK-8 method, morphological changes, and mitochondrial membrane potential were observed with an inverted microscope, cell cycle and cell apoptosis were examined by flow cytometry and DNA damages were detected by comet assay. Results Our results showed that cell viability was significantly decreased in a dose-dependent manner when concentration was higher than 0.2 mg/mL. A concentration above 1 mg/mL altered the cells morphology. Each DNA damage indicator score increased in the groups with the concentration of above 0.1 mg/mL. Cells at G2/M phase, cell apoptosis and mitochondrial membrane potential changed in the 2 mg/mL group. Conclusion Overall, our study suggests that CR at a high dosage exhibits cytotoxicity on L929 cells, which is likely to be the consequences of cell cycle arrest, DNA damage, cell apoptosis and mitochondrial membrane potential reduction.