Type 2 diabetes is associated with oxidative stress and low-grade inflammation resulting in endothelial dysfunction (ED). This study determined to explore the protective effects of berry-derived anthocyanins (AC) with potent antioxidant and anti-inflammatory activities in human diabetic endothelial cells upon oxidative and inflammatory stressors. Cultured healthy human aortic endothelial cells (HAEC) and diabetic human aortic endothelial cells (D-HAEC) exposed to oxidative stress by hydrogen peroxide (H2O2, 75 μM) and lipopolysaccharide (LPS, 1 μg/mL) as an inflammatory inducer before treatment with AC (50 μl/ml). The results from cytotoxicity assays showed that AC had no significant effects in cell viability (P-value < 0.0001), and exposure to H2O2 75 μM had a less toxic effect (P-value < 0.05). Although, AC significantly decreased H2O2-induced cytotoxicity and oxidative stress in both HAEC and D-HAEC cell lines (P-value < 0.0001), no positive impact of AC was found on the GSSG/GSH ratios (P-value < 0.05). Exposure to the LPS increased the production of IL-6 in both HAEC and D-HAEC cell lines (P-value < 0.0001), whereas AC treatment reduced LPS-induced IL-6 production in both cell lines with a more robust impact on D-HAEC (P-value < 0.0001). While LPS increased inflammasome assembling and caspase-1 activation, AC treatment inhibited caspase-1 activation in D-HAEC (P ≤ 0.05). This study indicated that berry anthocyanins reduced oxidative stress and inflammation via the inhibition of the NF-ƙB signaling pathway, which contributes to mitigating the diabetes-induced up-regulation of NF-ƙB.

中文翻译：

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浆果花色苷对人原发性糖尿病主动脉内皮细胞中诱导的氧化应激和炎症的细胞保护作用。

2型糖尿病与氧化应激和轻度炎症相关，导致内皮功能障碍（ED）。这项研究旨在探讨浆果衍生的花色苷（AC）在人的糖尿病内皮细胞中对氧化应激和炎症应激的有效保护作用。培养的健康人主动脉内皮细胞（HAEC）和糖尿病人主动脉内皮细胞（D-HAEC）在过氧化氢（H2O2，75μM）和脂多糖（LPS，1μg/ mL）暴露于氧化应激后暴露于氧化应激AC（50μl/ ml）。细胞毒性试验的结果表明，AC对细胞活力无明显影响（P值<0.0001），而暴露于75μMH2O2的毒性较小（P值<0.05）。虽然，在HAEC和D-HAEC细胞系中，AC显着降低H2O2诱导的细胞毒性和氧化应激（P值<0.0001），而AC对GSSG / GSH比率没有积极影响（P值<0.05）。暴露于LPS可增加HAEC和D-HAEC细胞系中IL-6的产生（P值<0.0001），而AC处理可降低LPS诱导的两种细胞系中IL-6的产生，并对D产生更强烈的影响-HAEC（P值<0.0001）。尽管LPS增加了炎症小体的组装和caspase-1的激活，但是AC处理抑制了D-HAEC中caspase-1的激活（P≤0.05）。这项研究表明，浆果花色苷可通过抑制NF-ƙB信号通路来减少氧化应激和炎症反应，这有助于减轻糖尿病引起的NF-ƙB的上调。