The impact of chronic blackberry intake on the neuroinflammatory status of rats fed a standard or high-fat diet

 

Neuroinflammation has been suggested as a centralmediator of central nervous systemdysfunction, including in dementia and neurodegenerative disease. Flavonoids have emerged as promising candidates for the prevention of neurodegenerative diseases and are thought to be capable of antiinflammatory effects in the brain. In the present study, the impact of a chronic intake of an anthocyanin extract fromblackberry (BE) on brain inflammatory status in the presence or absence of a high-fat dietwas investigated. Following intake of the dietary regimes for 17 weeks neuroinflammatory status in Wistar rat cortex, hippocampus and plasma were assessed using cytokine antibody arrays. In the cortex, intake of the high-fat diet resulted in an increase of at least 4-fold, in expression of the cytokine-induced neutrophil chemoattractant CINC-3, the ciliary neurotrophic factor CNTF, the platelet-derived growth factor PDGF-AA, IL-10, the tissue inhibitor of metalloproteinase TIMP-1 and the receptor for advanced glycation end products RAGE. BE intake partially decreased the expression of these mediators in the high-fat challenged brain. In standard-fed animals, BE intake significantly increased cortical levels of fractalkine, PDGF-AA, activin, the vascular endothelial growth factor VEGF and agrin expression, suggesting effects as neuronal growth and synaptic connection modulators. In hippocampus, BE modulates fractalkine and the thymus chemokine TCK-1 expression independently of diet intake and, only in standard diet, increased PDGF-AA. Exploring effects of anthocyanins on fractalkine transcription using the neuronal cell line SH-SY5Y suggestedthat other cell types may be involved in this effect. This is the first evidence, in in vivo model, that blackberry extract intake may be capable of preventing the detrimental effects of neuroinflammation in a high-fat challenged brain. Also, fractalkine and TCK-1 expression may be specific targets of anthocyanins and their metabolites on
neuroinflammation.

 

神经炎症被认为是中枢神经系统功能障碍的中枢介质，包括痴呆和神经退行性疾病。类黄酮已经成为预防神经退行性疾病的有前途的候选物质，并被认为具有抗大脑炎症作用。在目前的研究中，研究了在高脂肪饮食存在或不存在的情况下，长期摄入黑莓花青素提取物(BE)对脑炎症状态的影响。通过细胞因子抗体阵列检测Wistar大鼠皮层、海马和血浆的神经炎症状态。在皮层中，摄入高脂肪食物导致细胞因子诱导的中性粒细胞趋化剂c5 -3、睫状神经营养因子CNTF、血小板源性生长因子PDGF-AA、IL-10、金属蛋白酶组织抑制剂TIMP-1和晚期糖基化终末产物RAGE受体。BE的摄入部分地降低了高脂肪大脑中这些介质的表达。在标准饲养的动物中，摄入BE显著提高了皮质fractalkine、PDGF-AA、激活素、血管内皮生长因子VEGF和agrin的表达水平，表明其作为神经元生长和突触连接调节因子的作用。在海马中，BE调节fractalkine和胸腺趋化因子TCK-1的表达，而不依赖于饮食摄入，并且仅在标准饮食中增加PDGF-AA。利用神经细胞系SH-SY5Y探索花青素对fractalkine转录的影响，提示其他类型的细胞可能参与了这种影响。这是第一个证据，在体内模型，黑莓提取物摄入可能能够防止神经炎症的有害影响高脂肪挑战的大脑。此外，fractalkine和TCK-1的表达可能是花青素及其代谢产物对神经炎症的特异性靶点。

 

Read More

https://www.sciencedirect.com/science/article/abs/pii/S0955286315001412