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Bioactivities and action mechanisms of active compounds from Hottuynia cordata Thunb on human lung cancer cells

BACKGROUND: Lung cancer is the leading cause of death in Taiwan for years. Besides the currently used chemotherapy, herbal medicine may play a role in the treatment of lung cancer. Hottuynia cordata Thunb (HC), one of the frequently used herbal medicine in Taiwan, has been widely used in various dis...

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Detalles Bibliográficos
Autores principales: Chen, Yuh-Fung, Chang, Wen-Hsin, Tsai, Huei-Yann, Lee, Min-Min, Wu, Tian-Shang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: China Medical University 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8824244/
https://www.ncbi.nlm.nih.gov/pubmed/35223403
http://dx.doi.org/10.37796/2211-8039.1219
Descripción
Sumario:BACKGROUND: Lung cancer is the leading cause of death in Taiwan for years. Besides the currently used chemotherapy, herbal medicine may play a role in the treatment of lung cancer. Hottuynia cordata Thunb (HC), one of the frequently used herbal medicine in Taiwan, has been widely used in various diseases. Review from literatures, HC has many effects, including anti-inflammatory, anti-viral, anti-bacterial, anti-SARS, and anti-tumor activities. However, there is no literatures describe its active compounds on lung cancer. This present study aims to evaluate the possible effect and action mechanism of active compounds from HC (aristolactam BII, aristolactam AII, and noraristolodione) on lung cancer. A549 lung cancer cell line was used to evaluate the effects of HC on the cell viability and possible anti-tumor effects. METHODS: We used A549 cells in the evaluation of anticancer activity. Cell viability, cell cycle, cell apoptosis and apoptosis related protein expression were studied. RESULTS: Active compounds from HC significantly inhibited A549 cell viability and induced accumulation of cell cycle at S or G2/M phase on A549 cells in a concentration-dependent manner, and induced A549 arrest at S or G2/M phase via increasing p21, p27, p53 and reducing cyclin-E, -A, cyclin-dependent kinase 2 (CDK2), cdc-2 (CDK1) protein expression. Additionally, HC induced A549 cell late apoptosis by up-regulating caspase-3, -8, Bax and decreasing Bcl-2 protein expression. CONCLUSIONS: The anti-tumor effects of aristolactam BII, aristolactam AII, and noraristolodione on human lung carcinoma A549 cells were via cell cycle arrest and apoptosis.