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磷虾油水包油乳液可在体外保护巨噬细胞免受脂多糖诱导的促炎激活。

Krill Oil-In-Water Emulsion Protects against Lipopolysaccharide-Induced Proinflammatory Activation of Macrophages In Vitro.

作者信息

Bonaterra Gabriel A, Driscoll David, Schwarzbach Hans, Kinscherf Ralf

机构信息

Department of Medical Cell Biology, Philipps-University Marburg, Robert-Koch-Straße 8, 35032 Marburg, Germany.

Stable Solutions LLC, Easton Industrial Park, 19 Norfolk Avenue, South Easton, MA 02375, USA.

出版信息

Mar Drugs. 2017 Mar 15;15(3):74. doi: 10.3390/md15030074.

Abstract

BACKGROUND

Parenteral nutrition is often a mandatory therapeutic strategy for cases of septicemia. Likewise, therapeutic application of anti-oxidants, anti-inflammatory therapy, and endotoxin lowering, by removal or inactivation, might be beneficial to ameliorate the systemic inflammatory response during the acute phases of critical illness. Concerning anti-inflammatory properties in this setting, omega-3 fatty acids of marine origin have been frequently described. This study investigated the anti-inflammatory and LPS-inactivating properties of krill oil (KO)-in-water emulsion in human macrophages in vitro.

MATERIALS AND METHODS

Differentiated THP-1 macrophages were activated using specific ultrapure-LPS that binds only on the toll-like receptor 4 (TLR4) in order to determine the inhibitory properties of the KO emulsion on the LPS-binding capacity, and the subsequent release of TNF-α.

RESULTS

KO emulsion inhibited the macrophage binding of LPS to the TLR4 by 50% (at 12.5 µg/mL) and 75% (at 25 µg/mL), whereas, at 50 µg/mL, completely abolished the LPS binding. Moreover, KO (12.5 µg/mL, 25 µg/mL, or 50 µg/mL) also inhibited (30%, 40%, or 75%, respectively) the TNF-α release after activation with 0.01 µg/mL LPS in comparison with LPS treatment alone.

CONCLUSION

KO emulsion influences the LPS-induced pro-inflammatory activation of macrophages, possibly due to inactivation of the LPS binding capacity.

摘要

背景

肠外营养通常是败血症病例的一种强制性治疗策略。同样,通过去除或灭活来进行抗氧化剂的治疗应用、抗炎治疗和降低内毒素,可能有助于改善危重病急性期的全身炎症反应。关于这种情况下的抗炎特性,海洋来源的ω-3脂肪酸经常被提及。本研究在体外研究了磷虾油(KO)水包油乳液在人巨噬细胞中的抗炎和脂多糖(LPS)灭活特性。

材料和方法

使用仅与Toll样受体4(TLR4)结合的特定超纯LPS激活分化的THP-1巨噬细胞,以确定KO乳液对LPS结合能力的抑制特性,以及随后肿瘤坏死因子-α(TNF-α)的释放。

结果

KO乳液在12.5μg/mL时将LPS与TLR4的巨噬细胞结合抑制了50%,在25μg/mL时抑制了75%,而在50μg/mL时完全消除了LPS结合。此外,与单独的LPS处理相比,KO(12.5μg/mL、25μg/mL或50μg/mL)在用0.01μg/mL LPS激活后也分别抑制了30%、40%或75%的TNF-α释放。

结论

KO乳液影响LPS诱导的巨噬细胞促炎激活,可能是由于LPS结合能力的失活。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3482/5367031/cbca189ae4a4/marinedrugs-15-00074-g001.jpg

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