ArticleMolecular medicine reports2017
Niaspan inhibits diabetic retinopathy‑induced vascular inflammation by downregulating the tumor necrosis factor‑α pathway.
Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 9 citations in OpenAlex.
- The Role of Immune Cells and Signaling Pathways in Diabetic Eye Disease: A Comprehensive Review.Biomedicines · 2024Review
- Administration of Melatonin in Diabetic Retinopathy Is Effective and Improves the Efficacy of Mesenchymal Stem Cell Treatment.Stem cells international · 2022Article
- Sustained Inhibition of NF-κB Activity Mitigates Retinal Vasculopathy in Diabetes.The American journal of pathology · 2021Article
- Trimetazidine Increases Plasma MicroRNA-24 and MicroRNA-126 Levels and Improves Dyslipidemia, Inflammation and Hypotension in Diabetic Rats.Iranian journal of pharmaceutical research : IJPR · 2020Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetic retinopathy (DR) is a serious microvascular complication of diabetes and a major cause of blindness in the developing world. Early DR is characterized by vascular neuroinflammation, cell apoptosis and breakdown of the blood‑retinal barrier (BRB). However, optimal treatment options and associated mechanisms remain unclear. Niaspan, which is widely used in the prevention and treatment of hyperlipidemia‑associated diseases, has been reported to inhibit inflammation. However, the effects of Niaspan and the mechanisms underlying the anti‑inflammatory effects of Niaspan on DR have yet to be reported. The present study aimed to investigate the anti‑inflammatory effects and mechanisms of Niaspan in a rat model of DR. Rats with DR exhibited a significant increase in BRB breakdown, retinal apoptosis, and tumor necrosis factor‑α (TNF‑α) and nuclear factor‑κB (NF‑κB) expression. In addition, the expression levels of inducible nitric oxide synthase (iNOS) and intercellular cell adhesion molecule‑1 (ICAM‑1) were increased in the retinas of DR rats compared with in the normal control group. In conclusion, treatment with Niaspan significantly improved clinical and histopathological outcomes; decreased the expression levels of TNF‑α, NF‑κB, iNOS and ICAM‑1; and decreased apoptosis and BRB breakdown, as compared with in the retinas of DR rats. The present study is the first, to the best of our knowledge, to demonstrate that Niaspan treatment ameliorates DR by inhibiting inflammation, and also suggests that the TNF‑α pathway may contribute to the beneficial effects of Niaspan treatment.
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