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首页> 外文期刊>Cytokine >Ursolic acid exhibits anti-inflammatory effects through blocking TLR4-MyD88 pathway mediated by autophagy
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Ursolic acid exhibits anti-inflammatory effects through blocking TLR4-MyD88 pathway mediated by autophagy

机译：通过阻塞由自噬介导的TLR4-MYD88途径表现出抗炎作用

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摘要

There is an urgent need for effective treatments to reduce the large and growing burden of acute kidney injury (AKI) and its consequences. Inflammation is believed to play a vital role in the pathophysiology of AKI. Macrophage autophagy is considered protective against inflammation. Previous study discovered that ursolic acid (UA), a natural pentacyclic triterpene carboxylic acid found in many plants as apples, bilberries, cranberries and so on, promoted cancer cell autophagy. In the present study, we aimed to explore the effect of UA on ameliorating AKI and the role of macrophage autophagy in the context of inflammation. The data from in vivo experiments showed that pretreatment of mice with UA significantly suppressed xylene-induced ear oedema as well as protected against LPS-induced AKI. Related mechanisms were further studied through in vitro experiment. As expected, UA decreased inflammatory factors TNF-alpha, IL-6 and IL-1 beta secretion in macrophages in response to lipopolysaccharide (LPS) stimulation. Furthermore, UA blocked LPS-induced TLR4/MyD88 pathway. More importantly, enhanced autophagy of macrophages by UA through increasing the expression of both LC3B and Beclin-1 led to alter macrophage function. What is more, similar to UA, autophagy inhibitor 3-MA obviously decreased inflammation factors releases hinting the vital role of autophagy in regulating inflammation. In all, above study suggested that UA is a potential anti-inflammatory natural compound for treating AKI by inducing autophagy.
机译：迫切需要有效治疗，以减少急性肾损伤（AKI）的大量和不断增长的负担及其后果。据信炎症在Aki的病理生理学中发挥着至关重要的作用。巨噬细胞自噬被认为是对炎症的保护性。以前的研究发现，熊糖酸（UA），在许多植物中发现的天然五胞苷三萜羧酸，如苹果，越桔，蔓越莓等，促进癌细胞自噬。在本研究中，我们旨在探讨UA对改善AKI的影响以及巨噬细胞自噬在炎症背景下的作用。来自体内实验的数据表明，用UA的小鼠预处理明显抑制二甲苯诱导的耳朵水肿，并保护对抗LPS诱导的AKI。通过体外实验进一步研究了相关机制。正如预期的那样，uA响应于脂多糖（LPS）刺激，UA减少巨噬细胞中的炎症因子TNF-α，IL-6和IL-1β分泌。此外，UA阻断了LPS诱导的TLR4 / MYD88途径。更重要的是，通过增加LC3B和BECLIN-1的表达，通过增加LC3B和BECLIN-1的表达来增强巨噬细胞的自噬上，以改变巨噬细胞功能。更重要的是，类似于UA，自噬抑制剂3-mA明显降低炎症因子释放暗示自噬在调节炎症方面的重要作用。总而言之，上述研究表明，UA是通过诱导自噬治疗AKI的潜在的抗炎天然化合物。

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  • 来源
    《Cytokine》 |2019年第2019期|共8页
  • 作者

    Zhao Jun; Zheng Haoyi; Sui Zhongguo; Jing Fanbo; Quan Xianghua; Zhao Wenwen; Liu Guangwei;

  • 作者单位

    Qingdao Univ Affiliated Hosp Dept Pharm Qingdao Shandong Peoples R China;

    Qingdao Univ Coll Med 308 Ningxia Rd Qingdao 266021 Shandong Peoples R China;

    Qingdao Univ Affiliated Hosp Dept Pharm Qingdao Shandong Peoples R China;

    Qingdao Univ Affiliated Hosp Dept Pharm Qingdao Shandong Peoples R China;

    Qingdao Univ Affiliated Hosp Dept Pharm Qingdao Shandong Peoples R China;

    Qingdao Univ Coll Med 308 Ningxia Rd Qingdao 266021 Shandong Peoples R China;

    Qingdao Univ Affiliated Hosp Outpatient Dept Qingdao Shandong Peoples R China;

  • 收录信息
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 细胞生物学;
  • 关键词

    Inflammation; Autophagy; Macrophagy; Acute kidney injury;

    机译：炎症;自噬;巨乳;急性肾损伤;

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