Abstract
Vitis amurensis Rupr. “Beibinghong” is abundant in anthocyanins, including malvidin (Mv), malvidin-3-glucoside (Mv3G), and malvidin-3,5-diglucoside (Mv35 G). Anthocyanins offer nutritional and pharmacological effects, but their stability is poor. Interaction of malvid anthocyanins with caffeic acid through ultrahigh pressure technology produces stable anthocyanin derivatives. This study aims to identify the structure of stable mallow-like anthocyanins and to determine the effect of these stable anthocyanins on human umbilical vein endothelial cells (HUVECs) with H2O2-induced oxidative damage and the signaling pathway involved. The products of malvid anthocyanins and caffeic acid bonding were identified and analyzed using ultra-high performance liquid chromatography-quadrupole-Orbitrap mass spectrometry (UPLC-Q-Orbitrap MS/MS). The bonding products were malvidin-3-O-guaiacol (Mv3C), malvidin-3-O-(6″-O-caffeoyl)-glucoside (Mv3CG), and malvidin-3-O-(6″-O-caffeoyl)-5-diglucoside (Mv3C5G). An oxidative stress injury model in HUVECs was established using H2O2 and treated with Mv, Mv3G, Mv35 G, Mv3C, Mv3CG, and Mv3C5G at different concentrations (10, 50, and 100 μmol/L). Results showed that the above compound concentrations can significantly increase cell proliferation rate and reduce intracellular reactive oxygen species at 100 μmol/L. The effects of the most active products Mv and Mv3C on the AMP-activated protein (AMPK)/silencing information regulator-1 (SIRT1) pathway were analyzed. Results showed that Mv and Mv3C significantly increased SOD activity in the cells and significantly upregulated the expression of SIRT1 mRNA, SIRT1, and p-AMPK protein. However, they did not significantly change the expression of AMPK protein. After the silent intervention of siRNA in SIRT1 gene expression, the upregulation of SIRT1 and p-AMPK protein by Mv and Mv3C was significantly inhibited. These results indicate that stabilization malvid anthocyanins exerts an antioxidant activity via the AMPK/SIRT1 signaling pathway.
Highlights
Oxidative stress injury is an important risk factor for human aging, subhealth, and various diseases, such as tumors, diabetes, cardiovascular and cerebrovascular diseases, Alzheimer’s disease, and neuropathy. e body produces a large number of reactive oxygen species (ROS) during oxidative stress
Ultrahigh pressure can promote the mutual color of anthocyanins and organic acids in the grapevine in a short time, with a remarkable stabilizing effect [13]
According to literature [25], m/z 282.07894 may be the 0,3A+ free radical positive ions caused by the breaking of C-C bond on the 0/3 position of anthocyanin C-ring, m/z 121.02881 is caused by the fragment ion m/z 282.07894 losing one molecular mass residue of 162 glucose, and the caffeoyl group may be linked to the glucoside at position 3
Summary
Oxidative stress injury is an important risk factor for human aging, subhealth, and various diseases, such as tumors, diabetes, cardiovascular and cerebrovascular diseases, Alzheimer’s disease, and neuropathy. e body produces a large number of reactive oxygen species (ROS) during oxidative stress. E body produces a large number of reactive oxygen species (ROS) during oxidative stress. In addition to direct damage to cells, ROS can activate different oxidative stress pathways, affecting the degree of tissue or cell damage. Oxidative stress can directly or indirectly activate AMP-activated protein (AMPK) through ROS or reactive nitrogen species. AMPK is a key protein involved in multiple signal transduction pathways, and AMPK signaling pathway imbalance is closely related to oxidative stress [1,2,3,4]. Recent studies have shown that the AMPK/SIRT1 signaling pathway is closely related to oxidative stress, aging, diabetes, and tumors [7,8,9,10]
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