Next Article in Journal
Rainbow Trout Red Blood Cells Exposed to Viral Hemorrhagic Septicemia Virus Up-Regulate Antigen-Processing Mechanisms and MHC I&II, CD86, and CD83 Antigen-presenting Cell Markers
Next Article in Special Issue
Methylglyoxal Acts as a Tumor-Promoting Factor in Anaplastic Thyroid Cancer
Previous Article in Journal
Protein Hydroxylation by Hypoxia-Inducible Factor (HIF) Hydroxylases: Unique or Ubiquitous?
Previous Article in Special Issue
Antiglycative Activity and RAGE Expression in Rett Syndrome
Open AccessArticle

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
*
Author to whom correspondence should be addressed.
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)
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
Show Figures

Figure 1

MDPI and ACS Style

Borriello, M.; Iannuzzi, C.; Sirangelo, I. Pinocembrin Protects from AGE-Induced Cytotoxicity and Inhibits Non-Enzymatic Glycation in Human Insulin. Cells 2019, 8, 385.

Show more citation formats Show less citations formats
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Access Map by Country/Region

1
Search more from Scilit
 
Search
Back to TopTop