| Literature DB >> 32325089 |
Rabia Nabi1, Sahir Sultan Alvi1, Mohammad Shafi Shah2, Saheem Ahmad1, Mohammad Faisal3, Abdulrahman A Alatar3, M Salman Khan4.
Abstract
Non-enzymatic protein glycation results in the formation of advanced glycation end products (AGEs) leads to the pathogenesis of long-term diabetic complications. Iridin (ID), an antioxidant, plays an important role in protecting against oxidative stress and could therefore be an efficacious anti-glycating regimen. Herein, we assessed the anti-glycating potential of ID against d-ribose induced glycation of bovine serum albumin (BSA) by various biophysical and biochemical techniques. Our results from several physicochemical assays advocated that ID was able to evidently prevent the AGEs generation via reducing hyperchromicity, early glycation products (EGPs), carbonyl content (CC), hydroxymethyl furfural (HMF) content, production of fluorescent AGEs, protection against loss of secondary structure (i.e. α-helix and β-sheets) of proteins, increasing the free lysine and free arginine content, reduced binding of congo red (CR), and reduced thioflavin T (ThT) and 8-aninilo-1-napthalene sulphonate (ANS)-specific fuorescence in glycated-BSA (Gly-BSA). On the basis of these findings, we concluded that ID possesses the significant anti-glycation potential and may be established as a remarkable anti-AGEs therapeutic agent. Further in-vivo and clinical studies are still warranted to uncover the therapeutic effects of ID against age-related as well as metabolic diseases.Entities:
Keywords: Advanced glycation end-products (AGEs); BSA; Glycation; Iridin; d-Ribose
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Year: 2020 PMID: 32325089 DOI: 10.1016/j.abb.2020.108373
Source DB: PubMed Journal: Arch Biochem Biophys ISSN: 0003-9861 Impact factor: 4.013