School of Marine Sciences, Ningbo University, Ningbo 315211, China; College of Biological and Environmental Sciences, Zhejiang Wanli University, Ningbo 315100, China.
College of Biological and Environmental Sciences, Zhejiang Wanli University, Ningbo 315100, China.
Chin J Nat Med. 2020 Oct;18(10):749-759. doi: 10.1016/S1875-5364(20)60015-2.
This study aimed to investigate the effects of Sargassum fusiforme polysaccharide (SFPS I, II, and III) on the apoptosis and regulation of human erythroleukemia (HEL) cells. The effect of different doses of SFPS on HEL cell growth was detected using the Cell Counting Kit-8 method, and apoptosis was detected by Hoechst staining. Cell cycle distribution and apoptosis were detected using flow cytometry. Expression of the cell cycle gene, p53, antiapoptotic genes, Bcl-xL and Bcl-2, and pro-apoptotic genes, Bax, Bad, and Caspase-3, as well as the expression of the corresponding proteins, were detected using real-time quantitative polymerase chain reaction (qPCR) and Western blot. The results showed that SFPS II and III decreased HEL cell viability and induced HEL cell apoptosis. Different concentrations of SFPS (I, II, and III) were detected that induced much less toxic effect in normal human embryonic lung (MRC-5) cells, and SFPS I increased cell proliferation, indicating its favorable selectivity towards cancer cells. The mechanism by which SFPS induced apoptosis was also found to be related to the induction of cell cycle arrest in the G/G phase and the increased expression of apoptosis-related genes and proteins. We concluded that SFPS induces HEL cell apoptosis, possibly via activation of the Caspase pathway, providing the theoretical basis for the development of SFPS-based anti-tumor drug products.
本研究旨在探讨半叶马尾藻多糖(SFPS I、II 和 III)对人红白血病(HEL)细胞凋亡和调控的影响。采用细胞计数试剂盒-8 法检测不同剂量 SFPS 对 HEL 细胞生长的影响,采用 Hoechst 染色法检测细胞凋亡。采用流式细胞术检测细胞周期分布和细胞凋亡。采用实时定量聚合酶链反应(qPCR)和 Western blot 检测细胞周期基因 p53、抗凋亡基因 Bcl-xL 和 Bcl-2 以及促凋亡基因 Bax、Bad 和 Caspase-3 的表达及其相应蛋白的表达。结果表明,SFPS II 和 III 降低 HEL 细胞活力并诱导 HEL 细胞凋亡。检测到不同浓度的 SFPS(I、II 和 III)对正常人类胚胎肺(MRC-5)细胞的毒性作用较小,SFPS I 增加细胞增殖,表明其对癌细胞具有良好的选择性。SFPS 诱导细胞凋亡的机制也与诱导细胞周期阻滞在 G/G 期和增加凋亡相关基因和蛋白的表达有关。我们得出结论,SFPS 诱导 HEL 细胞凋亡,可能通过激活 Caspase 途径,为开发基于 SFPS 的抗肿瘤药物提供了理论依据。