Curcumin prevents high glucose damage in retinal pigment epithelial cells through ERK1/2‐mediated activation of the Nrf2/HO‐1 pathway. Issue 10 (15th February 2019)

• Record Type: Journal Article
• Authors: Bucolo, Claudio; Drago, Filippo; Maisto, Rosa; Romano, Giovanni Luca; D'Agata, Velia; Maugeri, Grazia; Giunta, Salvatore
• Is Part Of: Journal of cellular physiology. Volume 234:Issue 10(2019:Oct.)
• Page Start: 17295
• Page End: 17304
• Publication Date: 2019-02-15
• Subjects: apoptosis -- curcumin -- diabetic retinopathy (DR) -- heme oxygenase‐1 (HO‐1) -- retinal pigment epithelial (RPE) cells; Physiology -- Periodicals; Cell physiology -- Periodicals; 571.6
• DOI: 10.1002/jcp.28347
• Languages: English
• ISSNs: 0021-9541

Abstract

Abstract: To study the effects of curcumin on human retinal pigment epithelial (RPE) cells exposed to high glucose (HG) insult, we performed in vitro studies on RPE cells cultured both in normal and HG conditions to assess the effects of curcumin on the cell viability, nuclear factor erythroid 2‐related factor 2 (Nrf2) expression, HO‐1 activity, and ERK1/2 expression. RPE cells exposed to HG insult were treated with curcumin. The cell viability, apoptosis, HO‐1 activity, ERK, and Nrf2 expression were evaluated. The data indicated that treatment with curcumin caused a significant decrease in terms of apoptosis. Further, curcumin was able to induce HO‐1 expression via Nrf2 activation and counteracts the damage elicited by HG. The present study demonstrated that curcumin provides protection against HG‐induced damage in RPE cells through the activation of Nrf2/HO‐1 signaling that involves the ERK pathway, suggesting that curcumin may have therapeutic value in the treatment of diabetic retinopathy. Abstract : Curcumin protects human retinal pigment epithelial (RPE) cells and induces the activation of nuclear factor erythroid 2‐related factor 2 (Nrf2)/HO‐1 signaling that involves the ERK pathway modulation.