Abstract

BACKGROUND:

Growing evidence suggests that hyperglycemia could be harmful for cognitive function. That insulin (INS) has a neuro-modulatory role is supported by various findings, but its effect on microglia, the innate immune cells in the brain, is largely unknown. Blueberries have been shown to reduce neuro-inflammation.

OBJECTIVE:

We hypothesized that high glucose stimulated an inflammation in microglia and that BB and INS were able to reduce it and both might act through GLUT-1 transporter.

METHODS:

We examined the effects of low (5 mM), medium (25 mM), or high (50 mM) glucose, stimulated or not with lipopolysaccharide (LPS; 100 nM) with either BB extract (2 mg/ml) and/or INS, on inflammatory responses in a microglia cell line. Nitric oxide (NO) production and the expression levels of iNOS, TNF-α, NOX4 and glucose transporter protein-1 (GLUT1) were assessed.

RESULTS:

We observed that treatment with BB, similarly to INS treatments, reduced the high glucose concentration-induced response on oxidative stress and inflammation, and that this protective effect is more important with LPS added to glucose media. Interestingly, both BB and INS attenuated the LPS-induced inflammatory response on GLUT1.

CONCLUSION:

Increasing glucose concentration triggers inflammation by microglia. BB as well as INS protected microglia from high glucose levels, by reducing inflammation and altering glucose transport in microglia. These preliminary data compared for the first time BB to Insulin on microglia. Blueberries are promising dietary intervention to prevent diabetic neuropathy. Our preliminary results suggest a possible new mechanism involving GLUT-1 by which BB has insulin-like effects.

中文翻译：

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蓝莓和胰岛素可保护小胶质细胞免受高糖诱导的炎症并恢复GLUT-1

摘要

背景：

越来越多的证据表明，高血糖症可能对认知功能有害。各种发现支持胰岛素（INS）具有神经调节作用，但对小胶质细胞（大脑中的先天免疫细胞）的作用尚不清楚。蓝莓已被证明可以减少神经炎症。

客观的：

我们假设高血糖会刺激小胶质细胞的炎症，而BB和INS能够减轻炎症，并且两者都可能通过GLUT-1转运蛋白起作用。

方法：

我们检查了用BB提取物（2 mg / ml）和/或INS用脂多糖（LPS; 100 nM）刺激或不刺激的低（5 mM），中（25 mM）或高（50 mM）葡萄糖的作用，关于小胶质细胞系中的炎症反应。评估一氧化氮（NO）的产生以及iNOS，TNF- α，NOX4和葡萄糖转运蛋白-1（GLUT1）的表达水平。

结果：

我们观察到，与INS治疗类似，BB治疗降低了高葡萄糖浓度引起的对氧化应激和炎症的反应，并且添加到葡萄糖培养基中的LPS的保护作用更为重要。有趣的是，BB和INS都减弱了LPS对GLUT1引起的炎症反应。

结论：

葡萄糖浓度增加会触发小胶质细胞的炎症。BB和INS通过减少炎症和改变小胶质细胞中的葡萄糖转运来保护小胶质细胞免受高葡萄糖水平的影响。这些初步数据首次将BB与小胶质细胞上的胰岛素进行了比较。蓝莓有望通过饮食干预来预防糖尿病性神经病变。我们的初步结果表明，涉及GLUT-1的新机制可能使BB具有类似胰岛素的作用。