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营养干预能否调节慢性肾脏病中 NLRP3 炎性体的激活?

Can nutritional interventions modulate the activation of the NLRP3 inflammasome in chronic kidney disease?

机构信息

Graduate Program in Medical Sciences, Fluminense Federal University (UFF), Niterói, Brazil.

Graduate Program in Cardiovascular Sciences, Fluminense Federal University (UFF), Niterói, Brazil.

出版信息

Food Res Int. 2020 Oct;136:109306. doi: 10.1016/j.foodres.2020.109306. Epub 2020 May 16.

Abstract

Inflammatory and innate immune responses triggered by pathogen-associated and other danger-associated signals emerging during infections, results in the activation of cytosolic inflammasomes. The nod-like receptor pyrin domain containing 3 (NLRP3) is one of the inflammasomes mediating such responses through the activation of caspase-1, which increases the production and release of pro-inflammatory cytokines, such as IL-1β and IL-18 and induces programmed cell death through pyroptosis. NLRP3 is thought to play a crucial role in the underlying inflammatory responses in many lifestyles related chronic diseases. Consequently, research on the NLRP3 inflammasome has expanded dramatically in recent years. Although several studies have investigated the role of NLRP3 activation in chronic kidney disease (CKD), few studies have evaluated strategies to modulate its activation by means of interventions using non-pharmacological strategies. This review discusses some nutritional strategies (bioactive compounds, probiotics and caloric restriction) that have been shown to influence NLRP3 in experimental models of renal disease, and in CKD. It discusses how nutritional interventions could potentially dampen NLRP3 associated inflammatory burden, as part of nutritional strategies to prevent and treat CKD and its complications.

摘要

在感染过程中,病原体相关和其他危险相关信号引发的炎症和先天免疫反应,导致细胞溶质炎性小体的激活。含吡咯并嘧啶结构域的 NOD 样受体 3(NLRP3)是介导此类反应的炎性小体之一,通过激活半胱天冬酶-1,增加促炎细胞因子(如 IL-1β 和 IL-18)的产生和释放,并通过细胞焦亡诱导程序性细胞死亡。NLRP3 被认为在许多与生活方式相关的慢性疾病的潜在炎症反应中发挥关键作用。因此,近年来 NLRP3 炎性小体的研究迅速扩展。尽管有几项研究调查了 NLRP3 激活在慢性肾脏病(CKD)中的作用,但很少有研究评估通过使用非药物策略的干预措施来调节其激活的策略。这篇综述讨论了一些营养策略(生物活性化合物、益生菌和热量限制),这些策略已被证明可影响肾脏疾病的实验模型以及 CKD 中的 NLRP3。它讨论了营养干预如何潜在地减轻 NLRP3 相关的炎症负担,作为预防和治疗 CKD 及其并发症的营养策略的一部分。

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