ArticleJournal, genetic engineering & biotechnology2023
Experimental and hypothetical appraisal on inhibition of glucose-induced glycation of bovine serum albumin by quercetin.
Article in Journal, genetic engineering & biotechnology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed, 3 citations in OpenAlex.
- Neuroprotective potential of quercetin in Alzheimer's disease: targeting oxidative stress, mitochondrial dysfunction, and amyloid-β aggregation.Frontiers in pharmacology · 2025Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe specificity of protein functions depends on its folding ability into a functional structure. Protein folding is an essential systemic phenomenon that prevents incorrect folding which could result in harmful aggregation. This harmful aggregation of proteins causes neurodegenerative diseases and systemic amyloidosis. Experimental and theoretical approaches were used in this study to explicate the probable mechanisms of action of quercetin in inhibition of glucose-induced glycation through estimations of percentage glycated protein, inhibited induced protein aggregation, and unoxidized bovine serum albumin thiol groups and assessments of molecular interactions of quercetin with the structures of bovine serum albumin, amyloid beta-peptide (1-42) and 3D amyloid-beta (1-42) fibrils retrieved from the protein databank ( http://www.rcsb.org ).
resultsThe results showed quercetin inhibited the formation of glycated protein, protein aggregation, and thiol oxidation in a concentration-dependent manner where 200 μg/ml showed the highest inhibition while 50 μg/ml depicted the least inhibition in all the studied assessments. From the docking analysis, it was observed that quercetin had a significantly higher binding affinities - 8.67 ± 0.09 kcal/mol, - 5.37 ± 0.05 kcal/mol and - 5.93 ± 0.13 kcal/mol for the bovine serum albumin, amyloid beta-peptide (1-42) and 3D amyloid-beta (1-42) fibrils respectively compared to the glucose, the inducer. Quercetin and glucose interacted with amino acid residues at the BSA subdomain IIA thus providing a clue that quercetin may impose its inhibition through the binding domain. Also, it is important to mention that the phytochemicals shared a similar interaction profile as that of glucose with the amyloid-beta.
conclusionsThese findings established the beneficial effects of quercetin as a potential agent that could alleviate hyperglycaemic-initiated disorders associated with elevated serum glucose levels.
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