Cellular and Molecular Biology Research Center, Health Research Institute, Babol University of Medical Sciences, Babol, Iran.
Department of Pharmacology and Toxicology, Faculty of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran.
Anticancer Agents Med Chem. 2022;22(4):721-730. doi: 10.2174/1871520621666210706142157.
Various plant species have been shown to be effective in the prevention or adjuvant therapy of cancer. Alpinia officinarum and its main phytochemicals have also been the subject of several studies for their anticancer properties.
The objective of this study is to analyze the extracts of A. officinarum to quantify flavonoids and to evaluate the growth inhibitory effects of the extracts on MCF-7 and LNCaP cells.
A. officinarum aqueous and hydroalcoholic extracts were analyzed by using High-Performance Liquid Chromatography (HPLC) for the quantification of three flavonoid compounds. Then, MCF-7, LNCaP, and fibroblast cells were treated with several concentrations (25, 50, 100, 200, and 400 μg/mL) of extracts (24, 48 and 72h). Cell viability was assessed using an MTT assay. Flow cytometry was conducted to evaluate apoptosis.
Galangin and kaempferol (3.85 and 1.57 mg/g dry extract) were quantified, respectively, in hydroalcoholic and aqueous extracts using a validated method. The hydroalcoholic extract significantly decreased the viability of MCF-7 (IC50: 43.45μg/mL for 48h) and LNCaP cells (IC50: 168 μg/mL for 48h). The aqueous extract reduced cancer cell viability by more than 50% only at 200 and 400 μg/mL (72 h). Treatment of primary fibroblasts with both extracts showed no significant decrease in cell viability (25-100 μg/mL; 24 and 48h). The hydroalcoholic extract induced a significant increase in apoptotic cells in both MCF-7 and LNCaP cells.
Obtained results demonstrated the cytotoxicity of A. officinarum through apoptosis induction in two cancer cell lines. Further investigations are required to determine the underlying apoptotic cell death mechanisms induced by A. officinarum in cancerous cells.
各种植物物种已被证明在预防或辅助癌症治疗方面有效。高良姜及其主要植物化学物质也因其抗癌特性而成为多项研究的主题。
本研究旨在分析高良姜提取物以定量黄酮类化合物，并评估提取物对 MCF-7 和 LNCaP 细胞的生长抑制作用。
使用高效液相色谱法（HPLC）分析高良姜的水提物和水醇提物，以定量三种黄酮类化合物。然后，用不同浓度（25、50、100、200 和 400μg/mL）的提取物（24、48 和 72h）处理 MCF-7、LNCaP 和成纤维细胞。使用 MTT 测定法评估细胞活力。通过流式细胞术评估细胞凋亡。
用验证方法分别定量了水醇提物中的高良姜素和山柰酚（分别为 3.85 和 1.57mg/g 干提取物）。水醇提物显著降低 MCF-7（48h 的 IC50：43.45μg/mL）和 LNCaP 细胞（48h 的 IC50：168μg/mL）的活力。水提物仅在 200 和 400μg/mL（72h）时使癌细胞活力降低 50%以上。两种提取物处理原代成纤维细胞时，细胞活力均无明显下降（25-100μg/mL；24 和 48h）。水醇提物诱导 MCF-7 和 LNCaP 细胞中凋亡细胞的显著增加。
研究结果表明，高良姜通过诱导两种癌细胞系的细胞凋亡来发挥细胞毒性作用。需要进一步研究以确定高良姜在癌细胞中诱导的细胞凋亡死亡机制。
