TLR4/NF-κB-NLRP3炎症小体信号通路在实验性自身免疫性前列腺炎大鼠中的作用机制  

Exploring mechanism of TLR4/NF-κB-NLRP3 inflammasome signaling pathway in experimental autoim-mune prostatitis rats

作　　者：陆良喜 史宏[1] 黄志敏[2] 陆杰[1] 王文杰 LU Liangxi;SHI Hong;HUANG Zhimin;LU Jie;WANG Wenjie(Department of Androl-ogy,Ren'ai Branch of the First Affiliated Hospital of Guangxi University of Chinese Medicine,Nanning 530001,Guangxi,China;不详)

机构地区：[1]广西中医药大学第一附属医院仁爱分院男科,广西南宁530001 [2]广西中医药大学第一附属医院风湿病科,广西南宁530023 [3]广西中医药大学基础医学院,广西南宁530001

出　　处：《实用医学杂志》2025年第6期800-805,共6页The Journal of Practical Medicine

基　　金：国家自然科学基金青年科学基金项目(编号:82205118);广西自然科学基金项目(编号:2020GXNSFBA297101)。

摘　　要：目的基于TLR4/NF-κB-NLRP3炎症小体信号通路探讨EAP大鼠发病机制。方法将12只SD雄性大鼠数字表随机分为正常组(N)、模型组(M)、Caspase-1抑制剂组(Caspase-1)、NLRP3抑制剂MCC950组(NLRP3),每组3只。药物干预后,采用HE染色、ELISA、WB法等观察相关指标。结果与N组比较,M组大鼠前列腺腺体结构损伤明显,炎症细胞浸润。与M组比较,Caspase-1组、NLRP3组前列腺腺体结构损伤减轻。与N组比较,M组大鼠前列腺组织TLR4、P-NF-κB P65、NLRP3、ASC、Cleaced-Caspase-1、Cleaced-IL-1β、IL-18蛋白表达升高(P<0.01)。与M组比较,NLRP3组、Caspase-1组TLR4、P-NFκB P65、Cleaced-Caspase-1、NLRP3、ASC、Cleaced-IL-1β、IL-18蛋白表达降低(P<0.01)。与N组比较,M组大鼠血清炎症因子IL-1β、IL-6、IFN-γ、IL-8、IL-18、IL-17A、TNF-α水平升高(P<0.01);血清IL-10水平略低,无统计学意义。与M组比较,Caspase-1组、NLRP3组大鼠血清IL-1β、IL-6、IL-8、IL-17A、IL-18、IFN-γ、TNF-α水平显著下降(P<0.05或P<0.01);血清IL-10水平升高(P<0.01)。结论TLR4/NF-κB-NLRP3炎症小体信号通路激活后促进EAP大鼠前列腺炎症的发生发展。Objective The pathogenesis of EAP in rats based on the TLR4/NF-κB-NLRP3 inflammasome signaling pathway was explored.Methods Randomly divide 12 male SD rats into 4 groups using the number table,namely normal group(N),model group(M),Caspase-1 inhibitor group(Caspase-1),and NLRP3 inhibitor MCC950 group(NLRP3),with 3 rats in each group.After drug intervention,relevant indicators were observed by using HE staining,ELISA,WB methods.Results Compared with the N group,the M group rats had showed significant damage in prostate gland structure and infiltration of inflammatory cells.Compared with group N,the expression of TLR4,P-NF-κB P65,NLRP3,ASC,Cleaced-Caspase-1,Cleaced-IL-1β,and IL-18 proteins in the prostate tissue of group M rats had increased(P<0.01).Compared with group M,the expression of TLR4,P-NF-κB P65,NLRP3,ASC,Cleaced-Caspase-1,Cleaced-IL-1β,and IL-18 proteins in the NLRP3 and Caspase-1 groups had significantly reduced(P<0.01).The serum levels of IL-1β,IL-6,IL-8,IL-17A,IL-18,IFN-γ,and TNF-αin group M rats had been significantly higher than those in group N(P<0.01).But the serum levels of IL-10 had been slightly lower and no statistical significance.The serum levels of IL-1β,IL-6,IL-8,IL-17A,IL-18,IFN-γ,and TNF-αin group M rats had been lower than those in group N(P<0.01 or P<0.05),the serum IL-10 level had increased(P<0.01).Conclusion The activation of TLR4/NF-κB-NLRP3 inflammasome signaling pathway promotes the occurrence and development of prostatitis in EAP rats.

关 键 词：慢性前列腺炎 慢性盆腔疼痛综合征 NLRP3炎症小体 TLR4/NF-κB-NLRP3炎症小体信号通路 炎症因子 

分 类 号：R697.33[医药卫生—泌尿科学]