The attenuating effects of 1,2,3,4,6 penta-O-galloyl-β-d-glucose on inflammatory cytokines release from activated BV-2 microglial cells.
The attenuating effects of 1,2,3,4,6 penta-O-galloyl-β-d-glucose on inflammatory cytokines release from activated BV-2 microglial cells.
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DOI：
10.1016/j.jneuroim.2017.01.011
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发表时间：
2017-04-15
影响因子：
3.3
通讯作者：
Soliman KF
中科院分区：
文献类型：
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作者：
Mendonca P;Taka E;Bauer D;Cobourne-Duval M;Soliman KF
阿尔茨海默病（AD）是老年人神经退行性变和痴呆的最常见原因。小胶质细胞（脑的常驻巨噬细胞）的失调的慢性活化诱导过量的促炎细胞因子的释放，这已经涉及AD病理的早期阶段。因此，抑制这些炎症介质的表达可能会减少或延缓AD的进展。许多来自植物的天然化合物已显示出抗炎活性。天然存在的1，2，3，4，6-五-O-没食子酰基-β-D-葡萄糖（PGG）是盐肤木中高度富集的多酚类化合物。它是一种有效的抗炎剂，在不同的实验模型中通过抑制许多细胞因子发挥作用。在本研究中，我们研究了PGG作为抗炎剂在LPS/IFNγ激活的BV-2小胶质细胞中的作用。使用小鼠细胞因子抗体阵列来评估PGG对促炎细胞因子释放的影响，并进行ELISA实验以验证来自阵列的结果。从细胞因子阵列和ELISA测定获得的结果显示，PGG使单核细胞趋化蛋白-5（MCP-5）的表达降低8倍，使基质金属蛋白酶原9（Pro MMP-9）的表达降低10倍。这两种细胞因子在炎症过程中上调，并已被证明参与脑损伤，炎症和神经变性。因此，这些发现表明PGG对活化的小胶质细胞的抗炎作用涉及MCP-5和ProMMP-9细胞因子的衰减。
Alzheimer’s disease (AD) is the most common cause of neurodegeneration and dementia in the elderly. Dysregulated, chronic activation of microglia, the brain’s resident macrophages, induces the release of excessive amounts of pro-inflammatory cytokines which has been implicated in the early stages of AD pathology. Therefore, suppressing the expression of these inflammatory mediators may decrease or delay the progression of AD. Many natural compounds derived from plants have shown anti-inflammatory activity. The naturally occurring 1,2,3,4,6 Penta-O-Galloyl-β-D-Glucose (PGG), is a polyphenolic compound highly enriched in Rhus chinensis Millplant. It is a potent anti-inflammatory agent that act through the inhibition of many cytokines in different experimental models. In the present study, we investigated the role of PGG as an anti-inflammatory agent in LPS/IFNγ activated BV-2 microglia cells. Mouse cytokine antibody arrays were used to assess the effect of PGG on the release of pro-inflammatory cytokines, and ELISA experiments were performed to validate the results from the arrays. The results obtained from the cytokine arrays, and ELISA assays showed that PGG decreased the expression of monocyte chemotactic protein-5 (MCP-5) 8-fold, and pro-matrix metalloproteinase 9 (Pro MMP-9) 10-fold. Both of these cytokines are upregulated during the inflammatory process and have been shown to be involved in brain injury, inflammation, and neurodegeneration. Therefore, these findings suggest that the anti-inflammatory effect of PGG on activated microglia involving the attenuation of MCP-5 and ProMMP-9 cytokines.