Soltan Maha M, Abd-Alla Howaida I, Hassan Amal Z, Hanna Atef G
Biology Unit, Central Laboratory for Pharmaceutical and Drug Industries Research Division, Chemistry of Medicinal Plants Department, National Research Centre, El Buhouth St. 33Dokki-Giza12622, Egypt.
Chemistry of Natural Compounds Department, Pharmaceutical and Drug Industries Research Division, National Research Centre, El Buhouth St. 33, Dokki-Giza12622, Egypt.
Z Naturforsch C J Biosci. 2021 Jun 1;76(7-8):337-346. doi: 10.1515/znc-2020-0302. Print 2021 Jul 27.
Acovenoside A (Acov-A) and acobioside A (Acob-A) were isolated from . Their anticancer properties were explored regarding, antiproliferative and antiangiogenic activities. The study included screening phase against six cancer cell lines followed by mechanistic investigation against HepG2 cancer cell line. The sulforhodamine-B (SRB) was used to determine their growth inhibitory power. In the other hand, flow cytometry techniques were recorded the cell death type and cell cycle analysis. The clonogenic (colony formation) and wound healing assays, enzyme-linked immunosorbent assay (ELISA) and molecular docking, were performed to evaluate the antiangiogenesis capability. Both compounds were strongly, inhibited four cancer cell lines at GI less than 100 nM. The mechanistic investigation against HepG2 resulted in cell accumulations at G2M phase and induction of apoptosis upon treating cells separately, with 400 nM Acov-A and 200 nM Acob-A. Interestingly, the same concentrations were able to activate caspase-3 by 7.2 and 4.8-fold, respectively. Suppressing the clonogenic capacity of HepG2 cells (20 and 40 nM) and inhibiting the migration of the colon Caco-2 cancer cells were provoke the results of vascular endothelial growth factor receptor2 (VEGFR2) kinase enzyme inactivation. The docked study was highly supportive, to the antiangiogenic approach of both cardenolides. The isolated cardenolides could orchestrate pivotal events in fighting cancer.
从……中分离出了阿考糖苷A（Acov-A）和阿考二糖苷A（Acob-A）。研究了它们的抗癌特性，包括抗增殖和抗血管生成活性。该研究包括针对六种癌细胞系的筛选阶段，随后针对肝癌细胞系HepG2进行机制研究。使用磺酰罗丹明B（SRB）来确定它们的生长抑制能力。另一方面，采用流式细胞术记录细胞死亡类型和细胞周期分析结果。进行克隆形成（集落形成）和伤口愈合试验、酶联免疫吸附测定（ELISA）以及分子对接，以评估抗血管生成能力。两种化合物均能强烈抑制四种癌细胞系，其生长抑制浓度（GI）小于100 nM。对HepG2细胞系的机制研究表明，分别用400 nM的Acov-A和200 nM的Acob-A处理细胞后，会导致细胞在G2M期积累并诱导细胞凋亡。有趣的是，相同浓度的两种化合物分别能使半胱天冬酶-3激活7.2倍和4.8倍。抑制HepG2细胞的克隆形成能力（20和40 nM）以及抑制结肠癌细胞Caco-2的迁移，会导致血管内皮生长因子受体2（VEGFR2）激酶失活。对接研究高度支持这两种强心苷的抗血管生成方法。分离出的强心苷可能在抗癌过程中协调关键事件。
