These beneficial antidiabetic observations suggest that resveratrol may be considered as a therapeutic supplement to prevent from diabetic retinopathy.

The current study was designed to explore whether microRNA-146a and its adapter proteins (tumor necrosis factor (TNF) receptor-associated factor 6 (TRAF6) and interleukin-1 receptor-associated kinase 1 (IRAK1)) are involved in the pathogenesis of diabetes neuropathy. Twelve male Sprague Dawley rats were randomized into control and diabetic groups (n = 6). Diabetes was induced by a single-dose injection of nicotinamide (110 mg/kg; i.p.), 15 min before injection of streptozotocin (50 mg/kg; i.p.) in 12-h-fasted rats. Diabetic neuropathy was evaluated by hot plate and tail emersion tests, 2 months after the injection of streptozotocin. The gene expression level of microRNA-146a (miR-146a), IRAK1, TRAF6, and nuclear factor kappa B (NF-κB) was measured in the sciatic nerve of rats using the real time-PCR method. Moreover, the activity of NF-κB and the concentration of pro-inflammatory cytokines were determined by the ELISA method. In comparison with the control group, a threefold increase in the expression of miR-146a and NF-κB, and a twofold decrease in the expression of TRAF6 were observed in the sciatic nerve of diabetic rats. Furthermore, the NF-κB activity and the concentration of TNF-α, interleukin 6 (IL-6), and interleukin 1β (IL-1β) in the sciatic nerve of diabetic rats were higher than in those of control counterparts. These results suggest that a defect in the NF-кB-miR-146a negative feedback loop may be involved in the pathogenesis of diabetic neuropathy.

Abstract. This study was designed to investigate the possible effectiveness of chronic resveratrol administration on redox state, inflammatory mediators and apoptosis rate in diabetic rats. Male Wistar rats were divided into four groups (n = 6): normal control, diabetic control, normal rats treated with resveratrol, and diabetic rats treated with resveratrol. Diabetes was induced by injection of streptozotocin (50 mg/kg; i.p.), 15 min after the prescription of nicotinamide (110 mg/kg; i.p.) in 12 h-fasted rats. Four-month oral resveratrol administration (5 mg/kg/day) significantly alleviated hyperglycemia, weight loss, enhancement of oxidative markers (lipid peroxidation index, nitrite/nitrate content and oxidized to reduced glutathione ratio) and superoxide dismutase activity in diabetic rats. Moreover, resveratrol administration to diabetic rats improved the elevated levels of plasma TNFα and IL-6 as well as NF-κB activity of polymorphonuclear cells. On the other hand, four months resveratrol administration decreased the apoptosis rate in the kidney, heart, retina, sciatic nerve and the polymorphonuclear cells of diabetic rats. These beneficial antidiabetic observations suggest that treatment with resveratrol may be considered as a therapeutic approach to reduce diabetic-related complications.

8-isoprostane, 6.03 ± 0.87 vs. 8.49 ± 0.52 µmol, p < 0.05 for nitrite/nitrate, and 0.44 ± 0.03 vs. 0.59 ± 0.04, p < 0.05 for oxidized/reduced glutathione ratio), nuclear factor kappa B activity (0.37 ± 0.09 vs. 0.60 ± 0.11, p < 0.05) and apoptosis rate (0.98 ± 0.28 vs. 1.63 ± 0.16, p < 0.05). Moreover, it improved left ventricular developed pressure (72.46 ± 8.16 vs. 52.01 ± 11.32 mm Hg, p < 0.05) and coronary flow (14.08 ± 1.09 vs. 11.75 ± 1.43 mL/ /min × g, p < 0.05). Conclusions: These beneficial cardioprotective observations suggest that treatment with resveratrol can potentially delay or attenuate the progression of diabetes-related cardiac complications. (Cardiol J 2014; 21, 1: 39-46)

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