黄酮类化合物调节NLRP3炎性体:缓解糖尿病周围神经病变的一种有希望的方法。

IF 4.6 2区 医学 Q2 IMMUNOLOGY
Saumya Khanna, Sachindra Kumar, Pratyasha Sharma, Rajni Daksh, Krishnadas Nandakumar, Rekha Raghuveer Shenoy
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引用次数: 0

摘要

糖尿病常见且严重的副作用是糖尿病周围神经病变(DPN),其特征是由氧化应激、慢性炎症和长期高血糖引起的逐渐神经损伤。研究发现NLRP3炎症小体是DPN发病机制的关键介质,将神经炎症和神经元损伤与代谢衰竭联系起来。黄酮类化合物是一类天然存在的多酚类物质,由于其强大的抗炎和抗氧化特性,黄酮类化合物作为DPN的潜在治疗方法引起了人们的兴趣。本文综述了黄酮类化合物影响NLRP3炎性体的各种途径及其作为DPN治疗的潜力。研究表明,黄酮类化合物可以阻止NLRP3的激活,从而降低IL-1β和IL-18等促炎细胞因子的释放,导致神经炎症。黄酮类化合物通过减少氧化应激,改变重要的信号通路,阻断NF-κB和caspase-1的活性来发挥作用,这两种物质对NLRP3炎症小体的激活都是必不可少的。临床前研究表明,黄酮类化合物具有很强的神经保护作用,很少有临床证据表明黄酮类化合物具有改善糖尿病患者神经功能和减轻神经性疼痛的潜力。目前的综述强调了黄酮类化合物如何作为一种治疗策略来靶向NLRP3炎症小体引起的DPN炎症。通过靶向重要的炎症途径,类黄酮提供了一种减缓这种使人衰弱的疾病进展的新方法。进一步研究其作用机制、临床转化和新的给药技术,可以提高糖尿病周围神经病变的治疗效果。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Flavonoids regulating NLRP3 inflammasome: a promising approach in alleviating diabetic peripheral neuropathy.

A common and serious side effect of diabetes is diabetic peripheral neuropathy (DPN), which is characterised by gradual nerve damage brought on by oxidative stress, chronic inflammation, and prolonged hyperglycemia. Studies identify NLRP3 inflammasome as a key mediator in the pathogenesis of DPN, connecting neuroinflammation and neuronal damage to metabolic failure. Because of their strong anti-inflammatory and antioxidant qualities, flavonoids, a broad class of naturally occurring polyphenols, have drawn interest as potential treatments for DPN. The various ways that flavonoids affect the NLRP3 inflammasome and their potential as a treatment for DPN are examined in this review. It has been demonstrated that flavonoids prevent NLRP3 activation, which lowers the release of pro-inflammatory cytokines including IL-1β and IL-18 and causes neuroinflammation. Flavonoids work mechanistically by reducing oxidative stress, altering important signalling pathways, and blocking the activities of NF-κB and caspase-1, which are both essential for the activation of the NLRP3 inflammasome. Preclinical research has shown that flavonoids have strong neuroprotective benefits, and few clinical evidence also points to the potential of flavonoids to improve nerve function and lessen neuropathic pain in diabetic patients. The current review emphasises how flavonoids may be used as a treatment strategy to target inflammation in DPN caused by the NLRP3 inflammasome. By targeting important inflammatory pathways, flavonoids provide a new way to slow the progression of this debilitating illness. Further investigation into the mechanisms, clinical translation, and novel drug delivery techniques could enhance the therapeutic efficacy of diabetic peripheral neuropathy.

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来源期刊
Inflammopharmacology
Inflammopharmacology IMMUNOLOGYTOXICOLOGY-TOXICOLOGY
CiteScore
8.00
自引率
3.40%
发文量
200
期刊介绍: Inflammopharmacology is the official publication of the Gastrointestinal Section of the International Union of Basic and Clinical Pharmacology (IUPHAR) and the Hungarian Experimental and Clinical Pharmacology Society (HECPS). Inflammopharmacology publishes papers on all aspects of inflammation and its pharmacological control emphasizing comparisons of (a) different inflammatory states, and (b) the actions, therapeutic efficacy and safety of drugs employed in the treatment of inflammatory conditions. The comparative aspects of the types of inflammatory conditions include gastrointestinal disease (e.g. ulcerative colitis, Crohn''s disease), parasitic diseases, toxicological manifestations of the effects of drugs and environmental agents, arthritic conditions, and inflammatory effects of injury or aging on skeletal muscle. The journal has seven main interest areas: -Drug-Disease Interactions - Conditional Pharmacology - i.e. where the condition (disease or stress state) influences the therapeutic response and side (adverse) effects from anti-inflammatory drugs. Mechanisms of drug-disease and drug disease interactions and the role of different stress states -Rheumatology - particular emphasis on methods of measurement of clinical response effects of new agents, adverse effects from anti-rheumatic drugs -Gastroenterology - with particular emphasis on animal and human models, mechanisms of mucosal inflammation and ulceration and effects of novel and established anti-ulcer, anti-inflammatory agents, or antiparasitic agents -Neuro-Inflammation and Pain - model systems, pharmacology of new analgesic agents and mechanisms of neuro-inflammation and pain -Novel drugs, natural products and nutraceuticals - and their effects on inflammatory processes, especially where there are indications of novel modes action compared with conventional drugs e.g. NSAIDs -Muscle-immune interactions during inflammation [...]
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