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M. Rema, C. Premanand, Z. Sameer Mahmood, D. Anitha, M. Balasubramanyam; Inhibitory Effect of Curcumin on Human Retinal Endothelial Cell Proliferation . Invest. Ophthalmol. Vis. Sci. 2004;45(13):470.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: Curcumin (diferuloylmethane) is a small–molecular weight compound that is isolated from turmeric (Curcuma longa Linn). Several studies have shown that Curcumin has an anti–inflammatory, antioxidant and anti–proliferative effect on tumour cells. To evaluate the effect of Curcumin on Human Retinal Endothelial Cell (HREC) proliferation under various conditions and its relation to intracellular Reactive Oxygen Species (iROS) production. Methods: HREC were isolated and cultured within 20 hours of postmortem from human donors (as per ethical committee approval) in a medium containing either 5.5mM or 25mM Glucose, 200µg AGE–Bovine Serum albumin (AGE–BSA) adduct. Curcumin was then added. AGE–albumin adduct was quantified spectrofluorimetrically at 348 nm and 416 nm. The proliferation was assessed using chromogenic Methyl Thiazol Tetrazolium bromide (MTT) dye and tube formation. The effect of curcumin on phorbol ester (PMA) stimulated Vascular Endothelial Growth Factor (VEGF) and Flk1/KDR expression was analyzed by western blot. In addition, ATP and phorbol ester induced iROS (using Dihydroxyrhodamine) was measured using fluorimetric analysis. Results: Curcumin inhibited retinal endothelial cell proliferation in a dose dependent manner i.e., 7%, 16% and 48% inhibition on treating with 10, 30 and 50 µM concentrations respectively. Curcumin also decreased cell proliferation in the presence of AGE–Albumin (p= 0.001) and high glucose (p=0.002). There was increased production of iROS by HRECs when stimulated with phorbol ester and ATP. This was significantly inhibited when curcumin was added. In addition, phorbol ester stimulated VEGF was decreased significantly. Conclusion: Our study showed that the inhibitory effect of curcumin on human retinal endothelial cell proliferation could be caused by a decrease in PKC activity through a decrease in iROS production and VEGF.
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