Chemical characteristics and cytoprotective activities of polysaccharide fractions from Athyrium Multidentatum (Doll.) Ching

被引:16
作者
Jing, Liang [1 ]
Sheng, Jiwen [1 ]
Jiang, Jingru [1 ]
Wang, Yang [1 ]
Shen, Xiaoyan [1 ]
Liu, Dongmei [1 ]
Zhang, Weifen [1 ]
Mao, Shumei [1 ]
机构
[1] Weifang Med Univ, Dept Pharm, Weifang 261053, Peoples R China
关键词
Athyrium Multidentatum (Doll.) Ching; Cytoprotective activity; Polysaccharide fraction; PI3K/Akt/FOXO3a pathway; Nrf2/HO-1; pathway; ANTIOXIDANT ACTIVITY; OXIDATIVE STRESS; SULFATED POLYSACCHARIDE; APOPTOSIS; INJURY; DEATH; CELLS;
D O I
10.1016/j.ijbiomac.2020.05.053
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Five polysaccharide fractions (PS-1, PS-2, PS-3, PS-4 and PS-5) were successfully isolated from Athyrium Multidentatum (Doll.) Ching by anion-exchange column chromatography. Their in vitro cytoprotective activities and the underlying mechanisms were explored in this paper. Chemical analysis suggested that the five polysaccharide fractions were heteropolysaccharides with different molecular weights and monosaccharide compositions. Treatment with these polysaccharide fractions could increase cell viabilities, superoxide dismutase/ catalase activities, nitric oxide contents, mitochondrial membrane potential levels and Bcl-2/Bax ratios, and reduce cell apoptosis, intracellular reactive oxygen species production and malondialdehyde contents in H2O2-damaged cells. Moreover, these polysaccharide fractions enhanced the mRNA expression levels of PI3K, Akt, FOXO3a, Nrf2 and HO-1 and PS-4 exhibited the most powerful effects on the mRNA expression of these genes. Current findings suggested that the polysaccharide fractions decreased H2O2-induced apoptosis of HUVECs. The activation of PI3K/Akt/FOXO3a and Nrf2/HO-1 signaling pathways might be involved in the protective mechanisms of the active fractions. The polysaccharides might be one of the key bioactive ingredients of Athyrium Multidentatum (Doll.) Ching for the treatment of oxidative damage. (C) 2020 Elsevier B.V. All rights reserved.
引用
收藏
页码:1227 / 1238
页数:12
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