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生物活性化合物作为 NLRP3 炎性小体抑制剂的潜在影响:最新进展。

Potential Impact of Bioactive Compounds as NLRP3 Inflammasome Inhibitors: An Update.

机构信息

Department of Pharmacy, Institute of Pharmaceutical Research, GLA University, Uttar Pradesh-281406, India.

Department of Computer Engineering & Applications, GLA University, Uttar Pradesh-281406, India.

出版信息

Curr Pharm Biotechnol. 2024;25(13):1719-1746. doi: 10.2174/0113892010276859231125165251.

Abstract

The inflammasome NLRP3 comprises a caspase recruitment domain, a pyrin domain containing receptor 3, an apoptosis-linked protein like a speck containing a procaspase-1, and an attached nucleotide domain leucine abundant repeat. There are a wide variety of stimuli that can activate the inflammasome NLRP3. When activated, the protein NLRP3 appoints the adapter protein ASC. Adapter ASC protein then recruits the procaspase-1 protein, which causes the procaspase- 1 protein to be cleaved and activated, which induces cytokines. At the same time, abnormal activation of inflammasome NLRP3 is associated with many diseases, such as diabetes, atherosclerosis, metabolic syndrome, cardiovascular and neurodegenerative diseases. As a result, a significant amount of effort has been put into comprehending the mechanisms behind its activation and looking for their specific inhibitors. In this review, we primarily focused on phytochemicals that inhibit the inflammasome NLRP3, as well as discuss the defects caused by NLRP3 signaling. We conducted an in-depth research review by searching for relevant articles in the Scopus, Google Scholar, and PubMed databases. By gathering information on phytochemical inhibitors that block NLRP3 inflammasome activation, a complicated balance between inflammasome activation or inhibition with NLRP3 as a key role was revealed in NLRP3-driven clinical situations.

摘要

炎症小体 NLRP3 包含一个衔接蛋白 ASC 和半胱氨酸蛋白酶募集域,一个含有吡喃结构域的受体 3,一个衔接蛋白 ASC 蛋白和一个附着核苷酸结构域亮氨酸丰富重复。有许多不同的刺激可以激活炎症小体 NLRP3。当被激活时,NLRP3 蛋白指定衔接蛋白 ASC。然后,ASC 蛋白招募半胱氨酸蛋白酶-1 蛋白,导致半胱氨酸蛋白酶-1 蛋白被切割并激活,从而诱导细胞因子的产生。同时,炎症小体 NLRP3 的异常激活与许多疾病有关,如糖尿病、动脉粥样硬化、代谢综合征、心血管疾病和神经退行性疾病。因此,人们投入了大量的精力来理解其激活的机制,并寻找其特定的抑制剂。在这篇综述中,我们主要关注抑制炎症小体 NLRP3 的植物化学物质,并讨论 NLRP3 信号引起的缺陷。我们通过在 Scopus、Google Scholar 和 PubMed 数据库中搜索相关文章,进行了深入的研究综述。通过收集抑制 NLRP3 炎症小体激活的植物化学抑制剂的信息,揭示了 NLRP3 作为关键作用的 NLRP3 炎症小体激活或抑制之间的复杂平衡在 NLRP3 驱动的临床情况下。

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