食品科学

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荔枝落果中A型低聚原花青素抑制类甜蛋白促炎机制

罗杨合1,曾诗蔼2,李洛欣3,谢翀3,闫景坤4,李玉婷4,罗英捷5,赵雷2   

  1. 1. 贺州学院
    2. 华南农业大学
    3. 华南农业大学食品学院
    4. 东莞理工学院
    5. 营家健康科技(广东)有限公司
  • 收稿日期:2023-07-08 修回日期:2023-09-22 出版日期:2023-10-08 发布日期:2023-10-08
  • 通讯作者: 赵雷
  • 基金资助:
    广西康养食品科学与技术重点实验室开放课题;东莞市重点领域研发项目;广东省自然科学基金项目;广州市科技计划项目; “十四五” 广东省农业科技创新十大主攻方向

Mechanism of A-type oligomeric proanthocyanidins in litchi fruitlet to reduce inflammation of litchi thaumatin-like protein

  • Received:2023-07-08 Revised:2023-09-22 Online:2023-10-08 Published:2023-10-08

摘要: 论文以荔枝落果中的A型低聚原花青素为研究对象,探讨其对荔枝类甜蛋白促炎的抑制机理。采用乙醇提取、大孔吸附树脂纯化以及制备液相等从荔枝落果中分离得到A型原花青素纯化物(A-type oligomeric proanthocyanidins,A-OPC),并对A-OPC结构鉴定,主要成分为原花青素A2、2个A型原花青素三聚体和1个A型四聚体,纯度达88.69%。利用荔枝类甜蛋白(Litchi thaumatin-like protein,LcTLP)诱导构建RAW264.7细胞炎症模型,A-OPC的添加可抑制LcTLP诱导RAW264.7细胞的一氧化氮、细胞炎症因子白细胞介素-6和肿瘤坏死因子-α的分泌,在120 μg/mL浓度下,抑制率分别可达58.38%、86.31%和39.80%(P<0.01)。蛋白免疫印迹分析发现,在120 μg/mL浓度下A-OPC可降低诱导型一氧化氮合酶和环氧合酶2的表达量,并显著降低p-65、IκBα、JNK、ERK和p-38的磷酸化水平,说明A-OPC通过下调核转录因子-κB和丝裂原活化蛋白激酶通路中下游蛋白的磷酸化水平,从而抑制LcTLP诱导的炎症反应。

关键词: 荔枝落果, A型低聚原花青素, 荔枝类甜蛋白, 抗炎机制

Abstract: The paper was based on the A-type oligomeric proanthocyanidins in litchi fruitlet and investigated the inhibition mechanism of pro-inflammation induced by litchi thaumatin-like protein (LcTLP). The A-type oligomeric proanthocyanidins (A-OPC) were isolated from the fruitlet of litchi using ethanol extraction, purification by macroporous absorbing resin and preparative liquid chromatography. The structure of A-OPC was identified as proanthocyanidin A2, two A-type proanthocyanidin trimers and one A-type tetramer, with a purity of 88.69%. The inflammatory cell model was constructed by LcTLP. The addition of A-OPC inhibited the secretion of nitric oxide, interleukin-6 and tumor necrosis factor-α in RAW264.7 cells at 120 μg/ mL, the inhibition rate could reach 58.38%, 86.31% and 39.80%, respectively (P < 0.01). Western blot showed that 120 μg/mL A-OPC reduced the expression of inducible nitric oxide synthase and cyclooxygenase-2 and significantly decreased the phosphorylation levels of p-65, IκBα, JNK, ERK and p-38. Therefore, A-OPC inhibited the phosphorylation levels of downstream proteins in the nuclear transcription factor-κB and mitogen-activated protein kinase pathways to inhibit the LcTLP-induced inflammatory response.

Key words: litchi fruitlet, A-type oligomeric proanthocyanidins, litchi thaumatin-like protein, anti-inflammation mechanism

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