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J Ethnopharmacol:中药通过抑制NLRP3炎症小体对缺血性脑卒中的调控

2022-06-14 August MedSci原创

许多研究表明,多种中药(TCM) 对 NLRP3 炎性体介导的缺血性脑损伤具有强大的神经保护能力。这些中药可以是中药方剂、中药材及其提取物、中药单体等形式。

中风是一个重要的全球公共卫生问题,发病率、死亡率和残疾率都很高。大约 75-80% 的中风被归类为缺血性中风 (IS)。在中国,IS 是成人死亡的主要原因。IS 每年新增病例超过 200 万例,给社会和经济造成巨大负担。炎症诱导的神经元死亡是 IS 中的一个关键事件。在这个过程中,缺血和缺氧触发了常驻炎症细胞(星形胶质细胞、小胶质细胞和内皮细胞)的快速激活和脑内细胞间核因子的易位,以促进促炎因子的成熟和释放

核苷酸结合寡聚化结构域样受体 (NLR) 在称为炎性体的多蛋白平台的组装中起主要作用。在 NLR 中,NLRP3 是 NLR 家族的一个亚型。NLRP3炎症小体导致活化的caspase-1产生大量炎症因子,引起神经炎症,参与IS的发生发展。靶向抑制 NLRP3 炎症小体的激活可以缓解炎症反应,促进神经细胞存活,达到神经保护作用。因此,为提高IS患者的功能恢复,迫切需要开发新的治疗靶点和有效药物。

中医药在 IS 的治疗中逐渐得到了系统的研究和应用。由于中医药的多靶点、多环节、多系统、多途径作用,在治疗包括IS在内的多种疾病方面具有独特优势。此外,中药对 IS 的治疗作用与 NLPR3 炎性体的调节密切相关,表明它们有可能成为一种新的 IS 治疗策略。

材料和方法:通过设置关键词“NLRP3炎症小体”和“中药”以及“缺血性中风”来回顾最近发表的文章;Pubmed 和 GeenMedical 中的“NLRP3 炎症小体”和“缺血性中风”以及“天然产物”等。结果:根据最近的研究,16个中药方剂(官方授权产品和临床有效中药方剂)、7种中草药提取物和29种中药单体通过抗炎、抗氧化应激、抗凋亡和抗氧化应激对IS具有保护作用。线粒体自噬作用。

综上所述,此综述对针对 NLRP3 治疗 IS 的处方、草药提取物和中药活性单体成分的应用文献进行了系统回顾。证明了 NLRP3 炎性体是缓解 IS 的关键靶点,为进一步应用中医药治疗IS提供参考。

 

原文:Tao YW, Yang L, Chen SY, Zhang Y, Zeng Y, Wu JS, Meng XL. Pivotal regulatory roles of traditional Chinese medicine in ischemic stroke via inhibition of NLRP3 inflammasome. J Ethnopharmacol. 2022 May 2;294:115316. doi: 10.1016/j.jep.2022.115316. Epub ahead of print. PMID: 35513214.

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  5. 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    2023-04-24 jj000001
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    2022-06-14 yvaine

    学习一下NLRP3炎症小体

    0

  9. 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    2022-06-14 屋顶瞄爱赏月

    签到学习

    0

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    2022-06-01 yuandd

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Blood:以NF-κB和Notch为靶点治疗淋巴瘤

近日,《血液》杂志上发表了一篇文章,提供了遗传学证据,表明在B细胞中同时激活NF-κB和Notch信号足以诱导B细胞淋巴瘤转化,并启动普通的祖细胞通过去分化转化成髓系,而非转分化。有趣的是,转化的髓细胞还可以进一步转化为髓细胞白血病,虽然发生频率较低。

Blood:在成人T细胞白血病/淋巴瘤中,IRF4和NF-κB形成一个前馈回路调控基因表达

中心点:在ATL细胞,IRF4和NF-κB形成一个前馈回路,协同调控基因的表达。IRF4和NF-κB结合在超级增强子丰富区域,调控重要致癌基因表达,包括MYC、CCR4和BIRC3。摘要:成人T细胞白血病/淋巴瘤(ATL)是一种来源于成熟CD4+T淋巴细胞的高侵袭性的恶性血液病。近期,研究人员发现,ATL细胞转录调控网络由两个致癌转录因子(IRF4和NF-κB)驱动。原发性ATL样本的基因表达谱显

Blood:自分泌LTA信号驱动霍奇金淋巴瘤的NF-κB和JAK-STAT活性以及髓系基因的表达

NF-κB的持续性激活是典型霍奇金淋巴瘤(cHL)中的恶性霍奇金/RS(HRS)细胞的标志。基因组损伤、EB病毒感染、可溶性因子和肿瘤微环境的相互作用都可导致激活。Linda von Hoff等人采用一种公正的方法来识别cHL细胞分泌的可激活NF-κB的关键因子,采用色谱和质谱分析培养的cHL细胞的分泌蛋白质组。研究人员明确了α淋巴毒素(LTA)是cHL细胞系的经典和非经典NF-κB信号自分泌和旁

J Endod:抑制NF-κB通路减弱实验性尖周损伤的进展

NF-κB是血管再生的一个重要调控因子,它涉及到B-cell lymphoma 2 (Bcl-2)和Bcl-2-associated X protein (Bax)信号通路。因此,抑制NF-κB可能会通过阻断血管再生减弱尖周损伤的进展。为此,这篇研究的目的是为了评估NF-κB抑制剂寡脱氧核苷酸(ODN)对实验性尖周损伤的影响。

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