Tao Gao,Shuang Liu,Huang-yang Luo,Ren Wu,Rui Yan,Ling-zhi He,Qing-yu Nie,Hua-li Tang,Guiju Sun
Chuanminshen violaceum , as a food and folk medicine, is cultivated and grown only in China. Its polysaccharides play an important role in medicinal benefits. Herein, crude C. violaceum polysaccharides (CVPs) were purified to yield two polysaccharide fractions (CVPs-1-G and CVPs-2-G) using DEAE Cellulose-52 and Sephadex G-100 column chromatography. Structural analyses indicated that both CVPs-1-G and CVPs-2-G were glucans with average molecular weights of 8.1 kDa and 187.5 kDa, respectively. The main chain of the major component (CVPs-1-G) might be composed of (1 → 4)-linked α-Glc p , and the branched-chain might be an α-Glc p → 4)-α-D-Glc p -(1 → 6)-α-D-Glc p -(1 → 4)-α-D-Glc p , which connected to the main chain through the O-6 position of → 3,6)-α-D-Glc p -(1 →. In addition, CVPs-1-G displayed ABTS, DPPH, and hydroxyl radical scavenging activity, as well as competitive inhibitory activities of α-amylase and non-competitive inhibitory activities of lipase and pepsin. According to molecular docking, its inhibitory activity on digestive enzyme might be caused by hydrogen bond and hydrophobic interaction between them. Thus, CVPs exhibit strong potential for use in functional foods and pharmaceuticals.
We isolated and purified a novel polysaccharide from the root of Chuanminshen violaceum , namely, Chuanminshen violaceumis polysaccharide (CVP) and confirmed its structure and molecular weight. Furthermore, in vivo experiment, CVP's protective effect against myocardial ischemia-reperfusion (I/R) injury in mice was evidenced by significantly reducing I/R-induced myocardial infarction (MI) size, decreasing the secretion of heart damage biomarkers, and improving cardiac function. Then, the myocardial anoxia/reoxygenation (A/R) injury model was established to mimic reperfusion injury. Noticeably, ferroptosis was the major death manner for A/R-damaged H9c2 cells. Meanwhile, CVP significantly inhibited ferroptosis by decreasing intracellular Fe 2+ level, enhancing GPX4 expression, and suppressing lipid peroxidation to confront A/R injury. In conclusion, CVP, with a clear structure, ameliorated I/R injury by inhibiting ferroptosis.
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