ArticleAmerican journal of translational research2025
Carnosic acid attenuates diabetic retinopathy via the SIRT1 signaling pathway: neuroprotection and endothelial cell preservation.
Article in American journal of translational research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed.
- Protective Effect of Natural Phenolic Acids, Rosmarinic Acid and Salvianolic Acid, Against Diabetic Atherosclerosis.International journal of molecular sciences · 2026Review
- The Japanese Macaque as a Diabetes Recipient Animal Model for Porcine Islet Xenotransplantation.MedComm · 2026Article
- The Role of Ferroptosis in Diabetes Pathogenesis: Therapeutic Implications of Hydrogen Sulfide and Its Reactive Metabolites.Antioxidants (Basel, Switzerland) · 2026Review
- Ferroptosis-Mediated Cell-Specific Damage: Molecular Cascades and Therapeutic Breakthroughs in Diabetic Retinopathy.Antioxidants (Basel, Switzerland) · 2025Review
- Ferroptosis in diabetes mellitus and its complications: overview of clinical and preclinical research.Cell death discovery · 2025Review
- Elucidating programmed cell death in diabetic retinal microangionopathy and neurodegeneration: unraveling molecular mechanisms and therapeutic actions of natural products.Inflammopharmacology · 2025Review
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo explore the therapeutic effects of Carnosic acid (CA) on diabetic retinopathy (DR), a complication of diabetes mellitus (DM) characterized by retinal neuronal damage induced by oxidative stress.
methodsDR was induced in rodent models via streptozotocin (STZ) administration, while human retinal microvascular endothelial cells (HRMECs) were cultured in high-glucose (HG) conditions. The effects of CA on oxidative stress, inflammation, and apoptotic signaling were evaluated by quantifying relevant biomarkers.
resultsCA treatment significantly increased the expression of sirtuin 1, which was reduced in both STZ-treated rats and HG-exposed HRMECs, as confirmed by polymerase chain reaction (PCR) analysis. CA alleviated oxidative stress, inflammation, and apoptosis in STZ-induced DR models. In vitro, CA exhibited a dose-dependent enhancement of SIRT1 expression, providing substantial protection against HG-induced damage in HRMECs. This protective effect involved the suppression of oxidative mediators, reduction of pro-inflammatory cytokine release, and inhibition of apoptotic pathways. Additionally, CA prevented retinal ferroptosis by activating the SIRT1/p53/solute carrier family 7 member 11 (SLC7A11) pathway both in vivo and in vitro.
conclusionThis study suggests that CA alleviates DR by activating SIRT1, leading to decreased inflammation, apoptosis, and oxidative stress.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.