Niaspan inhibits diabetic retinopathy‑induced vascular inflammation by downregulating the tumor necrosis factor‑α pathway.

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.