首页|NLRP3炎症小体与IL-1β、TNF-α在痛风性关节炎急性发作中的相关性研究

NLRP3炎症小体与IL-1β、TNF-α在痛风性关节炎急性发作中的相关性研究

扫码查看
目的 分析NOD-样受体热蛋白结构域相关蛋白3(NOD-like receptor pyrin domain containing 3,NLRP3)炎症小体与促炎因子白细胞介素(interleukin,IL)-1β、肿瘤坏死因子(tumor necrosis factor,TNF)-α在急性痛风性关节炎发病过程中的相关性.方法 选取2023年6月至2024年7月温州市中医院收治的急性痛风性关节炎76例患者为病例组,选择同期体检的53名健康者为对照组.通过实时荧光定量聚合酶链反应(real-time quantitative polymerase chain reaction,RT-PCR)监测NLRP3炎症小体、凋亡相关斑点样蛋白(apoptosis-associated speck-like protein,ASC)、半胱氨酸蛋白酶-1(Caspase-1)、IL-1β、IL-18 及 TNF-a 的 mRNA 表达水平,并使用酶联免疫吸附测定(enzyme-linked immunosorbent assay,ELISA)法检测上述蛋白的浓度.结果 病例组患者的尿酸、C反应蛋白(C-reactive protein,CRP)及红细胞沉降率(erythrocyte sedimentation rate,ESR)高于对照组(P<0.001),病例组患者的 NLRP3、ASC、Caspase-1 表达量高于对照组(P<0.001).病例组患者的IL-1β、IL-18与TNF-a的血清含量高于对照组(P<0.05).Pearson相关性结果表明,NLRP3炎症小体的活性与IL-1β、TNF-α水平呈正相关;多因素Logistic回归分析显示,尿酸、CRP、ESR、NLRP3、ASC、Caspase-1、IL-1β、IL-18及TNF-α均为痛风性关节炎急性发作的重要影响因子(P<0.05).结论 通过抑制NLRP3炎症小体的激活或其下游炎性因子的释放,可有效减轻痛风性关节炎的炎症反应,缓解症状和预防关节损伤.
Study on the correlation between NLRP3 inflammasome and IL-1β,TNF-α in acute attacks of gouty arthritis
Objective To analyze the correlation between NOD like receptor pyrin domain containing 3(NLRP3)inflammasome and pro-inflammatory factors interleukin(1L)-1 β and tumor necrosis factor(TNF)-α in the pathogenesis of acute gouty arthritis.Methods From June 2023 to July 2024,76 patients in Wenzhou Hospital of Traditional Chinese Medicine with acute gouty arthritis were selected as case group,and 53 healthy individuals as control group.The mRNA expression levels of NLRP3 inflammasome,apoptosis-associated speck-like protein(ASC),Caspase-1,IL-1β,IL-18,TNF-α were monitored using real-time fluorescence quantitative real-time fluorescence quantitative(PCR),and concentrations of these proteins were determined using enzyme-linked immunosorbent assay(ELISA).Results Age,gender,and other data were similar between both groups(P>0.05).levels of uric acid,C-reactive protein(CRP),and erythrocyte sedimentation rate(ESR)in case group were higher than those in control group(P<0.001).Expression of NLRP3,ASC,and Caspase-1 were also higher(P<0.001).Serum levels of IL-1β,IL-18,and TNF-α were higher in case group(P<0.05).NLRP3 inflammasome activity correlated positively with IL-1β and TNF-α.Multivariate Logistic regression showed uric acid,CRP,ESR,NLRP3,ASC,Caspase-1,IL-1 β,IL-18,and TNF-α were important factors for acute gouty arthritis attacks(P<0.05).Conclusion By inhibiting activation of NLRP3 inflammasome or release of downstream inflammatory factors,inflammatory response of gouty arthritis can be effectively reduced,thereby alleviating symptoms and preventing joint damage.

Gouty arthritisNLRP3 inflammasomeRelevance

曾笑帅、李慧辉、吴惠明、刘海峰

展开 >

温州市中医院骨科,温州 325000

瑞安市人民医院骨科,瑞安 325200

痛风性关节炎 NLRP3炎症小体 相关性

2024

中国现代医生
中国医学科学院

中国现代医生

影响因子:1.571
ISSN:1673-9701
年,卷(期):2024.62(35)