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核桃相关脂肪酸抑制 LPS 诱导的 BV-2 小胶质细胞活化。

Walnut-Associated Fatty Acids Inhibit LPS-Induced Activation of BV-2 Microglia.

机构信息

Neuroscience & Aging Laboratory, USDA-ARS, HNRCA at Tufts University, 711 Washington Street, Boston, MA, 02111, USA.

Department of Psychology, College of Natural, Behavioral, and Health Sciences, Simmons University, 300 The Fenway, Boston, MA, 02115, USA.

出版信息

Inflammation. 2020 Feb;43(1):241-250. doi: 10.1007/s10753-019-01113-y.

DOI:10.1007/s10753-019-01113-y
PMID:31741196
Abstract

Walnuts have high levels of the omega-3 fatty acid alpha-linolenic acid (C18:3n-3, ALA) and the omega-6 fatty acid linoleic acid (C18:2n-6, LA). Previous research has demonstrated that pre-treatment of BV-2 microglia with walnut extract inhibited lipopolysaccharide (LPS)-induced activation of microglia. As an extension of that study, the effects of walnut-associated fatty acids on BV-2 microglia were assessed. BV-2 murine microglia cells were treated with LA, ALA, or a combination of LA+ALA prior to or after exposure to LPS. Nitric oxide (NO) and tumor necrosis factor-alpha (TNF-alpha) were measured in cell-conditioned media. Cyclooxeganse-2 (COX-2) and inducible nitric oxide synthase (iNOS) expression were assessed in BV-2 microglia. Both LA and ALA protected against LPS-induced increases in NO, iNOS, COX-2, and TNF-alpha when used before LPS exposure. When BV-2 microglia were treated with fatty acids after LPS, only COX-2 and TNF-alpha were significantly attenuated by the fatty acids. There was no synergism of LA+ALA, as the LA+ALA combination was no more effective than LA or ALA alone. Fatty acids, like those found in walnuts, may protect against production of cytotoxic intermediates and cell-signaling molecules from microglia and may prove beneficial for preventing age- or disease-related neurodegeneration.

摘要

核桃含有高水平的ω-3 脂肪酸α-亚麻酸(C18:3n-3,ALA)和 ω-6 脂肪酸亚油酸(C18:2n-6,LA)。先前的研究表明,BV-2 小胶质细胞用核桃提取物预处理可抑制脂多糖(LPS)诱导的小胶质细胞激活。作为该研究的扩展,评估了与核桃相关的脂肪酸对 BV-2 小胶质细胞的影响。在 LPS 暴露之前或之后,用 LA、ALA 或 LA+ALA 处理 BV-2 小鼠小胶质细胞。在细胞条件培养基中测量一氧化氮(NO)和肿瘤坏死因子-α(TNF-α)。评估 BV-2 小胶质细胞中环氧化酶-2(COX-2)和诱导型一氧化氮合酶(iNOS)的表达。LA 和 ALA 均可防止 LPS 诱导的 NO、iNOS、COX-2 和 TNF-α增加,当在 LPS 暴露之前使用时。当 LPS 后用脂肪酸处理 BV-2 小胶质细胞时,只有 COX-2 和 TNF-α被脂肪酸明显减弱。LA+ALA 没有协同作用,因为 LA+ALA 组合不如 LA 或 ALA 单独有效。脂肪酸,如在核桃中发现的脂肪酸,可能有助于防止小胶质细胞产生细胞毒性中间产物和细胞信号分子,并且可能有助于预防与年龄或疾病相关的神经退行性变。

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