ArticleScientific reports2021
Rosmarinic acid inhibits DNA glycation and modulates the expression of Akt1 and Akt3 partially in the hippocampus of diabetic rats.
Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 15 citations in OpenAlex.
- The Transformative Role of Nanotechnology in the Management of Diabetes Mellitus: Insights from Current Research.Biomolecules · 2025Review
- Reversing Glycation with a Dietary Supplement Containing Rosemary Extract.The Journal of clinical and aesthetic dermatology · 2025Review
- Therapeutic Effects of Proanthocyanidins on Diabetic Erectile Dysfunction in Rats.International journal of molecular sciences · 2024Article
- Glycation-driven matrix crosslinking in cirrhosis.Nature biomedical engineering · 2023Article
- Advanced Glycation End-Products and Diabetic Neuropathy of the Retina.International journal of molecular sciences · 2023Review
- The role of dietary antioxidants in type 2 diabetes and neurodegenerative disorders: An assessment of the benefit profile.Heliyon · 2023Review
- Biomedical features and therapeutic potential of rosmarinic acid.Archives of pharmacal research · 2022Review
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Authors and funding
3 authors at 1 institution in 1 country.
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Abstract
Non-enzymatic glycation of DNA and the associated effects are among pathogenic factors in diabetes mellitus. Natural polyphenols have anti-diabetic activity. Herein, the protective role of one of the phytochemicals, rosmarinic acid (RA), was evaluated in glycation (with fructose) of human DNA and expression of Akt genes in the hippocampus of diabetic rats. In-vitro studies using fluorescence, agarose gel electrophoresis, fluorescence microscopy, and thermal denaturation analyses revealed that glycation causes DNA damage and that RA inhibits it. In-vivo studies were performed by induction of diabetes in rats using streptozotocin. The diabetic rats were given RA daily through gavage feeding. The expression of Akt genes (inhibitors of apoptosis) in the hippocampus was evaluated using RT-qPCR. In diabetic rats, Akt1 and Akt3 were significantly down-regulated compared to the control group. Treating the diabetic rats with RA returned the expression of Akt1 and Akt3 relatively to the normal condition. Past studies have shown that diabetes induces apoptosis in the hippocampal neurons. Given that glycation changes the genes expression and causes cell death, apoptosis of the hippocampal neurons can be due to the glycation of DNA. The results also suggest that RA has reliable potency against the gross modification of DNA under hyperglycemic conditions.
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