Institute for Viral Hepatitis, Key Laboratory of Molecular Biology for Infectious Diseases, Chinese Ministry of Education, Department of Infectious Diseases, Second Affiliated Hospital of Chongqing Medical University, Chongqing, 400010, China; Pediatric Research Institute, Children's Hospital of Chongqing Medical University, Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing, 400014, China; China International Science and Technology Cooperation Base of Child Development and Critical Disorders, Chongqing, 400014, China; Chongqing key laboratory of pediatrics, Chongqing, 400014, China.
Chongqing key laboratory of pediatrics, Chongqing, 400014, China.
Carbohydr Polym. 2019 Jun 1;213:361-369. doi: 10.1016/j.carbpol.2019.02.081. Epub 2019 Feb 25.
One water-soluble polysaccharide (AAP), with a molecular weight of 6.3 × 104 Da, was isolated from Artemisia annua L. Structrual analysis indicated that AAP was found to be a 1, 3-α-linked and 1, 3, 6-α-linked Glcp backbone, with a branch of 1, 6-α-linked Glcp and terminal 1-linked-L-Rhap along the main chain in a ratio of 1: 1: 1: 1. MTT assay showed that AAP reduced the cell viability of HepG2 cells in a concentration-dependent manner. DAPI staining and Flow cytometric analysis revealed that AAP suppressed cells proliferation, not most at least via inducing p65-dependent mitochondrial signaling pathway, as evidenced by more activation of caspase-3 and -9, down-regulation of Bcl-2 protein, up-regulation of Bax protein and release of cytochrome c from mitochondria into cytosol, as well as suppression of the nuclear factor-κB (NF-κB) p65. These data confirmed AAP inhibits HepG2 cell growth via inducing caspase-dependent mitochondrial apoptosis and inhibition of NF-κB p65.
从青蒿中分离得到一种水溶性多糖（AAP），其分子量为 6.3×104Da。结构分析表明，AAP 由 1,3-α-连接和 1,3,6-α-连接的 Glcp 主链组成，侧链为 1,6-α-连接的 Glcp 和末端 1-连接的-L-Rhap，比例为 1:1:1:1。MTT 检测表明 AAP 呈浓度依赖性降低 HepG2 细胞活力。DAPI 染色和流式细胞术分析表明，AAP 通过诱导 p65 依赖性线粒体信号通路抑制细胞增殖，至少不是最主要的途径，这可以通过 caspase-3 和 -9 的更多激活、Bcl-2 蛋白的下调、Bax 蛋白的上调以及细胞色素 c 从线粒体释放到细胞质来证实，同时还抑制了核因子-κB（NF-κB）p65。这些数据证实，AAP 通过诱导 caspase 依赖性线粒体凋亡和抑制 NF-κB p65 抑制 HepG2 细胞生长。
