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Abstract Title:

Naringin attenuates diabetic retinopathy by inhibiting inflammation, oxidative stress and NF-κB activationand.

Abstract Source:

Iran J Basic Med Sci. 2017 Jul ;20(7):813-821. PMID: 28852447

Abstract Author(s):

Lihua Liu, Zhongfu Zuo, Sijing Lu, Aihua Liu, Xuezheng Liu

Article Affiliation:

Lihua Liu

Abstract:

OBJECTIVES: Naringin, an essential flavonoid, inhibits inflammatory response and oxidative stress in diabetes. However, whether naringin has beneficial effects on diabetic retinopathy (DR) remains unknown.

MATERIALS AND METHODS: Streptozotocin (STZ, 65 mg/kg) was intraperitoneally injected into male rats (8 weeks old weighting 200-250 g) to establish diabetic model, then naringin (20, 40 or 80 mg/kg/day) was intraperitoneally injected into the diabetic rats for twelve weeks. Glial fibrillary acidic protein (GFAP) level, thickness of ganglion cell layer (GCL) and ganglion cell counts were assessed in diabetic retina. Naringin (50μM) that significantly inhibited high glucose (HG, 25 mM)-induced cell proliferation was used to treat rat Muller cell line (rMC1). Inflammatory response, oxidative stress and activation of nuclear factor kappa B (NF-κB) p65 were evaluated in retinaand in rMC1 cells.

RESULTS: Naringin alleviated DR symptoms as evidenced by the increased retinal ganglion cells and decreased GFAP level in rat retina. Naringin exhibited anti-inflammatory and antioxidative effects as confirmed by the down-regulated pro-inflammatory cytokines, tumor necrosis factor alpha (TNF-α), interleukin-1β (IL-1β) and interleukin-6 (IL-6), and the up-regulated antioxidants, glutathione (GSH), superoxide dismutase (SOD) and catalase (CAT) in DR rats. Moreover, we found that naringin inhibited HG-induced proliferation, abnormal inflammatory response and oxidative stress in rMC1 cells. In addition, the enhanced nuclear translocation of NF-κB p65 in diabetic rat retina and HG-induced rMC1 cells was suppressed by naringin.

CONCLUSION: Naringin attenuates inflammatory response, oxidative stress and NF-κB activation in experimental models of DR.

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