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胃蛋白酶-胰酶水解降低了富含 lunasin 的物质抑制人 THP-1 巨噬细胞中炎症小体激活的能力。

Pepsin-pancreatin hydrolysis reduced the ability of lunasin-enriched material to inhibit activation of the inflammasomes in THP-1 human macrophages.

机构信息

Department of Food Science, The University of Tennessee Institute of Agriculture, Knoxville, TN 37996, USA.

出版信息

Food Funct. 2017 Dec 13;8(12):4449-4458. doi: 10.1039/c7fo00992e.

Abstract

Inflammation caused by the NLRP3 inflammasome has been linked to many diseases. Lunasin is a bioactive peptide from soybeans with reported anti-inflammatory properties. The objective of this work was to determine the effect of pepsin-pancreatin hydrolysis (PPH) on the ability of lunasin-enriched preparation (LEP) to inhibit inflammasome activation in differentiated THP-1 human macrophages. THP-1 macrophages were treated with different concentrations of LEP (0.0625 to 0.25 mg mL), primed with 1 μg mL lipopolysaccharide for 6 h and activated by 5 mM adenosine triphosphate for 1 h. LEP reduced secretion of IL-1β and IL-18. In addition, LEP treatment inhibited the production of intracellular reactive oxygen species (ROS) in THP-1 human macrophages without affecting the expressions of NLRP3 and ASC proteins involved in inflammasomes. PPH reduced the ability of LEP to inhibit production of intracellular ROS. Our results showed that LEP inhibited activation of inflammasomes by reducing intracellular ROS in vitro which was reduced by PPH.

摘要

NLRP3 炎性小体引起的炎症与许多疾病有关。豆乳蛋白素是一种具有抗炎特性的大豆生物活性肽。本研究的目的是确定胃蛋白酶-胰酶水解(PPH)对富含豆乳蛋白素的制剂(LEP)抑制分化的 THP-1 人巨噬细胞炎性小体激活能力的影响。用不同浓度的 LEP(0.0625 至 0.25mg/mL)处理 THP-1 巨噬细胞,用 1μg/mL 脂多糖孵育 6 小时,然后用 5mM 三磷酸腺苷激活 1 小时。LEP 减少了 IL-1β 和 IL-18 的分泌。此外,LEP 处理抑制了 THP-1 人巨噬细胞中细胞内活性氧(ROS)的产生,而不影响参与炎性小体的 NLRP3 和 ASC 蛋白的表达。PPH 降低了 LEP 抑制细胞内 ROS 产生的能力。我们的结果表明,LEP 通过减少细胞内 ROS 的产生来抑制体外炎性小体的激活,而 PPH 降低了 ROS 的产生。

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