ArticleMolecular and cellular biochemistry2022
Punicalagin protects against the development of pancreatic injury and insulitis in rats with induced T1DM by reducing inflammation and oxidative stress.
Article in Molecular and cellular biochemistry, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 11 citations in OpenAlex.
- Polyphenol-Mediated Modulation of Oxidative Stress Pathways in Type 1 Diabetes: A Systematic Review.Antioxidants (Basel, Switzerland) · 2026Review
- Janus kinase and signal transducer and activator of transcription inhibitors in type 1 diabetes and immune checkpoint-related diabetes: current status and future perspectives.Frontiers in immunology · 2025Review
- The Impact ofAntioxidants (Basel, Switzerland) · 2023Review
- Article
- Fruit waste: a current perspective for the sustainable production of pharmacological, nutraceutical, and bioactive resources.Frontiers in microbiology · 2023Review
- Punicalagin Protects against the Development of Methotrexate-Induced Hepatotoxicity in Mice via Activating Nrf2 Signaling and Decreasing Oxidative Stress, Inflammation, and Cell Death.International journal of molecular sciences · 2022Article
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pancreatic inflammation and oxidative damage remain major concerns in type 1 diabetes mellitus (T1DM). Punicalagin, a major polyphenol in pomegranates, exhibited antioxidant and protective effects on several organs in case of T1DM; however, no study has yet explored the protective effects of punicalagin on the pancreas and islets of Langerhans. T1DM was induced by injecting 40 mg/kg streptozotocin (STZ) intraperitoneally. Punicalagin (1 mg/kg ip) was injected daily for 15 days after T1DM induction. In diabetic rats, punicalagin treatment lowered the levels of inflammatory biomarkers (monocyte chemoattractant protein-1 and C-reactive protein) and adhesion molecules (E-selectin, intercellular adhesion molecule, and vascular cell adhesion molecule) while activating myeloperoxidase activity. Treatment of diabetic rats with punicalagin improved glutathione content and superoxide dismutase, catalase, and glutathione peroxidase activities; upregulated serum paraoxonase-1 activity; and prevented the elevation lipid peroxidation and protein oxidation products in the pancreas. Furthermore, punicalagin protected the pancreas against STZ-induced histopathological alterations and increased immune-reactive β-cells while reducing leucocyte infiltration into the islets of Langerhans, leading to normalized blood glucose and insulin levels. These findings indicated that punicalagin might protect against the development of insulitis in T1DM. In conclusion, punicalagin exerts a strong protective effect on the pancreas against oxidative injury and inflammation in STZ-induced experimental T1DM. The present results recommend punicalagin as a potential adjuvant for reducing diabetes-associated insulitis.
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