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首页> 外文期刊>Chemico-biological interactions >Cytoprotective effects of berry anthocyanins against induced oxidative stress and inflammation in primary human diabetic aortic endothelial cells
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Cytoprotective effects of berry anthocyanins against induced oxidative stress and inflammation in primary human diabetic aortic endothelial cells

机译:浆浆化花青素对原发性糖尿病主动脉内皮细胞诱导氧化应激和炎症的细胞保护作用

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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 mu M) and lipopolysaccharide (LPS, 1 mu g/mL) as an inflammatory inducer before treatment with AC (50 mu l/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 mu M 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-kappa B signaling pathway, which contributes to mitigating the diabetes-induced up-regulation of NF-kappa B.
机译:2型糖尿病与氧化应激和低级炎症相关,导致内皮功能障碍(ED)。该研究确定浆果衍生的花青素(AC)对氧化和炎症压力源在人糖尿病内皮细胞中有效抗氧化和抗炎活性的保护作用。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)通过过氧化氢(H 2 O 2,75μm)和脂多糖(LPS,1μg/ ml)作为炎性诱导剂以前暴露于氧化应激。用AC(50μl/ ml)处理。细胞毒性测定的结果表明,AC在细胞活力(P值<0.0001)中没有显着影响,并且暴露于H 2 O 275μM具有较小的毒性作用(P值<0.05)。虽然AC显着降低了H62O2诱导的HAEC和D-HAEC细胞系中的细胞毒性和氧化应激(P值<0.0001),但在GSSG / GSH比率上没有发现AC的正撞击(P值<0.05)。暴露于LPS在HAEC和D-HAEC细胞系中增加IL-6(P值<0.0001),而AC治疗在两种细胞系中减少了LPS诱导的IL-6产生,对D具有更强大的影响-haec(p值<0.0001)。虽然LPS增加了炎症组装和Caspase-1活化,但AC处理在D-HAEC中抑制了Caspase-1的活化(P <= 0.05)。本研究表明,浆浆化花青素通过抑制NF-κB信令途径来降低氧化应激和炎症,这有助于减轻糖尿病诱导的NF-κB的上调。

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