4.7 Article

Rubia sylvatica anthocyanins protect retinal pigment epithelial cells from H2O2-induced oxidative damage

Journal

FOOD BIOSCIENCE
Volume 56, Issue -, Pages -

Publisher

ELSEVIER
DOI: 10.1016/j.fbio.2023.103088

Keywords

Rubia sylvatica; Anthocyanins; Retinal pigment epithelial cells; Oxidative stress; Signaling pathway

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Natural anthocyanins from Rubia sylvatica fruit have been found to have a protective effect against oxidative stress in retinal pigment epithelial cells. They reduce oxidation products, increase antioxidant enzyme activity, enhance cell viability, and decrease apoptosis. The mechanism involves the activation of protein kinase B (Akt) through its phosphorylation process.
Natural anthocyanins are thought to be protective to eye health due to their recognized antioxidant properties. In this study, the protective effect of Rubia sylvatica fruit anthocyanins against oxidative stress in retinal pigment epithelial (RPE) cells and its mechanism were studied. Overall, Rubia sylvatica anthocyanin extract (RAE), the main anthocyanins found in the RAE, namely Cyanidin-3-O-glucoside (C3G), Delphinidin-3-O-rutinoside (D3R), and Cyanidin-3-O-rutinoside (C3R) all reduced H2O2-induced oxidative stress by decreasing the levels of oxidation products and increasing the activity of antioxidant enzymes. RAE and the three main anthocyanins enhanced cell viability from 54.11% & PLUSMN; 4.03%-85.13% & PLUSMN; 2.37% (RAE), 82.70% & PLUSMN; 2.63% (C3G), 94.00% & PLUSMN; 2.11% (D3R) and 89.99% & PLUSMN; 1.34% (C3R), respectively. And the total apoptosis rate of ARPE-19 cells fell from 14.16% & PLUSMN; 0.86%-9.45% & PLUSMN; 0.22% (RAE), 7.28% & PLUSMN; 0.49% (C3G), 8.88% & PLUSMN; 0.21% (D3R) and 8.59% & PLUSMN; 0.12% (C3R), respectively. The anthocyanins promoted the activation of protein kinase B (Akt) by activating Akt's phosphorylation process to maintain the normal growth and metabolism of cells. These results validate the hypothesis that R. sylvatica anthocyanins may protect against H2O2-induced oxidative injury of RPE through an antioxidant mechanism.

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