학술논문
Effects of Coptis extract combined with chemotherapeutic agents on ROS production, multidrug resistance, and cell growth in A549 human lung cancer cells.
Document Type
Article
Author
Source
Subject
*HERBAL medicine
*REACTIVE oxygen species
*ANALYSIS of variance
*ANTINEOPLASTIC agents
*CAMPTOTHECIN
*COMBINATION drug therapy
*DRUG resistance
*FLUOROURACIL
*LUNG cancer
*CHINESE medicine
*PACLITAXEL
*RESEARCH funding
*SPECTROPHOTOMETRY
*DATA analysis software
*DESCRIPTIVE statistics
*
*
*
*
*
*
*
*
*
*
*
*
*
*
Language
ISSN
1749-8546
Abstract
Background: Non-small cell lung cancer is associated with high expression of multidrug resistance (MDR) proteins and low production of reactive oxygen species (ROS). Coptis extract (COP), a Chinese medicinal herb, and its major constituent, berberine (BER), have anticancer properties. This study aims to investigate the effects of COP and BER combined with chemotherapeutic agents, including fluorouracil (5-FU), camptothecin (CPT), and paclitaxel (TAX) on cell proliferation, ROS production, and MDR in A549 human non-small cell lung cancer cells. Methods: A549 cells were treated with different doses of COP and BER, combined with 5-FU, CPT, and TAX. Cell viability was measured by an XTT (2,3-bis-(2-methoxy-4- nitro-5-sulfophenyl)-2 H-tetrazolium-5-carboxanilide) assay. Intracellular ROS levels were determined by measuring the oxidative conversion of cell permeable 2′,7′- dichlorofluorescein diacetate to fluorescent dichlorofluorescein. MDR of A549 cells was assessed by rhodamine 123 retention assay. Results: Both COP and BER significantly inhibited A549 cell growth in a dose-dependent manner. Combinations of COP or BER with chemotherapeutic agents (5-FU, CPT, and TAX) exhibited a stronger inhibitory effect on A549 cell growth. In addition, COP and BER increased ROS production and reduced MDR in A549 cells. Conclusion: As potential adjuvants to chemotherapy for non-small cell lung cancer, COP and BER increase ROS production, reduce MDR, and enhance the inhibitory effects of chemotherapeutic agents on A549 cell growth. [ABSTRACT FROM AUTHOR]