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Acylated Anthocyanins From Black Carrots and Their Related Phenolic Acids Diminish Priming and Activation of the NLRP3 Inflammasome in THP‐1 Monocytes
Molecular Nutrition & Food Research ( IF 4.5 ) Pub Date : 2024-10-19 , DOI: 10.1002/mnfr.202400356
Inken Behrendt, Katharina Becker, Christof Björn Steingass, Ralf Schweiggert, Gabriela Michel, Elvira Friedrich, Daniela Grote, Zoe Martin, Hanna Pauline Dötzer, Mathias Fasshauer, Martin Speckmann, Sabine Kuntz

ScopeExcessive activation of the nucleotide‐binding oligomerization domain‐like receptor pyrin domain‐containing protein 3 (NLRP3) inflammasome contributes to chronic inflammation. Thus, targeting NLRP3 inflammasome activation by anthocyanins may prevent inflammatory diseases. Therefore, the present study determines the influence of a black carrot extract (BCE) with high amounts of acylated anthocyanins and their related phenolic acids on the NLRP3 inflammasome.Methods and resultsTHP‐1 monocytes are pretreated with a BCE, cyanidin‐3‐glucoside (C3G), or hydroxycinnamic acids. NLRP3 inflammasome assembly is initiated by priming THP‐1 monocytes with lipopolysaccharide and/or activating the NLRP3 inflammasome with nigericin. Flow cytometry is used to assess apoptosis‐associated speck‐like protein containing a caspase recruitment domain (ASC) speck formation, as well as ASC and NLRP3 protein expression. Caspase‐1 activity is measured using a bioluminescent assay, and cytokine concentrations are determined by enzyme‐linked immunosorbent assays (ELISA). C3G and phenolic acids diminish ASC and NLRP3 protein expression. In addition, C3G and phenolic acids attenuate ASC speck formation. Furthermore, the BCE and C3G decline caspase‐1 activity. Consistently, IL‐1β and IL‐18 secretion are reduced upon NLRP3 inflammasome activation.ConclusionThe present study shows that a BCE with high amounts of acylated anthocyanins and their related phenolic acids diminish priming and activation of the NLRP3 inflammasome in THP‐1 monocytes.

中文翻译:


来自黑胡萝卜及其相关酚酸的酰化花青素会减少 THP-1 单核细胞中 NLRP3 炎性小体的启动和激活



范围核苷酸结合寡聚结构域样受体 pyrin 结构域包含蛋白结构域的蛋白 3 (NLRP3) 炎性小体的过度激活会导致慢性炎症。因此,通过花青素靶向 NLRP3 炎性小体激活可以预防炎症性疾病。因此,本研究确定了含有大量酰化花青素及其相关酚酸的黑胡萝卜提取物 (BCE) 对 NLRP3 炎性小体的影响。方法和结果THP-1 单核细胞用 BCE、矢车菊素-3-葡萄糖苷 (C3G) 或羟基肉桂酸预处理。NLRP3 炎性小体组装是通过用脂多糖引发 THP-1 单核细胞和/或用黑合菌素激活 NLRP3 炎性小体来启动的。流式细胞术用于评估含有 caspase 募集结构域 (ASC) 斑点形成的细胞凋亡相关斑点样蛋白,以及 ASC 和 NLRP3 蛋白表达。使用生物发光测定法测量 Caspase-1 活性,并通过酶联免疫吸附测定 (ELISA) 测定细胞因子浓度。C3G 和酚酸会降低 ASC 和 NLRP3 蛋白的表达。此外,C3G 和酚酸可减弱 ASC 斑点的形成。此外,BCE 和 C3G 降低 caspase-1 活性。一致地,在 NLRP3 炎性小体激活后,IL-1β 和 IL-18 分泌减少。结论本研究表明,具有大量酰化花青素及其相关酚酸的 BCE 会减少 THP-1 单核细胞中 NLRP3 炎性小体的启动和激活。
更新日期:2024-10-19
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