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Pinocembrin Protects from AGE-Induced Cytotoxicity and Inhibits Non-Enzymatic Glycation in Human Insulin

Department of Precision Medicine, Università degli Studi della Campania “Luigi Vanvitelli”, Via L. De Crecchio 7, 80138 Naples, Italy
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Cells 2019, 8(5), 385; https://doi.org/10.3390/cells8050385
Received: 16 April 2019 / Accepted: 24 April 2019 / Published: 26 April 2019
(This article belongs to the Special Issue Glycation and Dicarbonyl Stress in Aging and Disease)
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Abstract

Advanced glycation end products (AGEs) are the end products of the glycation reaction and have a great importance in clinical science for their association with oxidative stress and inflammation, which play a major role in most chronic diseases, such as cardiovascular disease, neurodegenerative diseases, and diabetes. Their pathogenic effects are generally induced by the interaction between AGEs and the receptor for advanced glycation end product (RAGE) on the cell surface, which triggers reactive oxygen species production, nuclear factor kB (NF-kB) activation, and inflammation. Pinocembrin, the most abundant flavonoid in propolis, has been recently proven to interfere with RAGE activation in Aβ–RAGE-induced toxicity. In the present study, we investigated the ability of pinocembrin to interfere with RAGE signaling pathways activated by AGEs. Interestingly, pinocembrin was able to inhibit oxidative stress and NF-kB activation in cells exposed to AGEs. In addition, it was able to block caspase 3/7 and 9 activation, thus suggesting an active role of this molecule in counteracting AGE–RAGE-induced toxicity mediated by NF-kB signaling pathways. The ability of pinocembrin to affect the glycation reaction has been also tested. Our data suggest that pinocembrin might be a promising molecule in protecting from AGE-mediated pathogenesis. View Full-Text
Keywords: advanced glycation end products (AGEs); oxidative stress; dicarbonyl stress; glycation; human insulin; AGE–RAGE pathways; pinocembrin advanced glycation end products (AGEs); oxidative stress; dicarbonyl stress; glycation; human insulin; AGE–RAGE pathways; pinocembrin
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Borriello, M.; Iannuzzi, C.; Sirangelo, I. Pinocembrin Protects from AGE-Induced Cytotoxicity and Inhibits Non-Enzymatic Glycation in Human Insulin. Cells 2019, 8, 385.

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