文章摘要
姚燕箐,汪焱,徐文静,等.异落新妇苷通过调节NLRP3炎症小体和NF-κB信号通路减轻尿酸钠诱导的小鼠急性痛风性关节炎机制研究[J].浙江中医药大学学报,2022,46(9):929-935, 944.
异落新妇苷通过调节NLRP3炎症小体和NF-κB信号通路减轻尿酸钠诱导的小鼠急性痛风性关节炎机制研究
Mechanism Study of Isoastilbin on Attenuating MSU-Induced Acute Gouty Arthritis in Mice Through Modulating NLRP3 Inflammasome and NF-κB Signaling Pathway
DOI:10.16466/j.issn1005-5509.2022.09.001
中文关键词: 异落新妇苷  急性痛风性关节炎  尿酸钠  踝关节肿胀  炎症因子  NLRP3炎症小体  NF-κB信号通路  机制研究
英文关键词: isoastilbin  acute gouty arthritis  MSU  ankle swelling  inflammatory factor  NLRP3 inflammasome  NF-κB signaling pathway  mechanism research
基金项目:国家自然科学基金项目(82074085 81673656);浙江省自然科学址金项(211H000;浙江中医药大学省重点建设高校优势特色学科(中药学)开放基金重点项目(ZYAOXZD2019002)
作者单位
姚燕箐 浙江中医药大学药学院 杭州 310053 
汪焱 浙江中医药大学药学院 杭州 310053 
徐文静 浙江中医药大学药学院 杭州 310053 
吴晨曦 浙江中医药大学药学院 杭州 310053 
楚秉泉 浙江中医药大学药学院 杭州 310053 
夏道宗 浙江中医药大学药学院 杭州 310053 
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中文摘要:
      [目的] 基于NOD样受体蛋白3(NOD-like receptor pyrin domain 3,NLRP3)炎症小体和核因子-κB(nuclear factor-κB,NF-κB)信号通路,研究异落新妇苷(isoastilbin,IA)对小鼠急性痛风性关节炎模型的抗炎作用及机制。[方法] 通过关节腔注射尿酸钠(monosodium urate,MSU)混悬液,建立小鼠急性痛风性关节炎模型,以自制足趾容积测量装置测定踝关节肿胀度;苏木精-伊红(hematoxylin-eosin,HE)染色法观察踝关节炎性浸润情况;酶联免疫吸附试验(enzyme linked immunosorbent assay,ELISA)检测踝关节中白细胞介素-1β(interleukin-1β,IL-1β)、白细胞介素-6(interleukin-6,IL-6)、肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)的水平;免疫印迹法检测踝关节中NLRP3炎症小体和NF-κB信号通路中相关蛋白的表达情况。 [结果] 踝关节注射MSU混悬液诱导小鼠产生急性痛风性关节炎。与正常组比较,模型组小鼠踝关节肿胀率明显升高(P<0.01),炎性浸润增加,IL-1β、IL-6、TNF-α分泌水平显著增高(P<0.01),NLRP3炎症小体和NF-κB信号通路相关蛋白表达增加(P<0.01)。与模型组比较,IA具有较强的抗炎效果,剂量依赖性地降低小鼠踝关节肿胀率(P<0.05,P<0.01),减轻炎性浸润情况,减少相关炎症因子的分泌(P<0.01),下调NLRP3炎症小体和NF-κB信号通路相关蛋白表达(P<0.01)。 [结论] IA对小鼠急性痛风性关节炎模型表现出较强的抗炎效果,其机制与调节NLRP3炎症小体和NF-κB信号通路相关。
英文摘要:
      [Objective] To study the anti-inflammatory effect and mechanism of isoastilbin(IA) on acute gouty arthritis in mice based on NOD-like receptor pyrin domain 3(NLRP3) inflammasome and nuclear factor-κB(NF-κB) signaling pathway. [Methods] The acute gouty arthritis model in mice was established by injecting monosodium urate(MSU) suspension into the articular cavity. Ankle swelling rate was measured by self-made toe volume installation; the state of inflammatory infiltration within ankle was observed through hematoxylin-eosin (HE) staining; the level of interleukin-1β (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α) secreted from ankle was determined by enzyme linked immunosorbent assay(ELISA); the expression of protein in ankle linked to NLRP3 inflammasome and NF-κB signaling pathway was detected by Western blot. [Results] MSU suspension was injected into ankle induced acute gouty arthritis in mice. Compared with normal group, the swelling rate of ankle in model group was significantly increased(P<0.01), inflammatory infiltration was increased, the secretion level of IL-1β, IL-6 and TNF-α was significantly increased(P<0.01), and the expression of NLRP3 inflammasome and NF-κB signaling pathway related proteins were increased(P<0.01). Compared with model group, IA had a good anti-inflammatory effect. IA reduced the swelling rate of ankle in a dose-dependent manner(P<0.05, P<0.01), alleviated inflammatory infiltration, reduced the secretion of related inflammatory cytokines(P<0.01), and down-regulated the expression of NLRP3 inflammasome and NF-κB signaling pathway related proteins(P<0.01). [Conclusion] IA has a strong anti-inflammatory effect in mice on acute gouty arthritis, and its mechanism is related to the regulation of NLRP3 inflammasome and NF-κB signaling pathway.
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