中国比较医学杂志2025，Vol.35Issue(4)：21-30,10.DOI:10.3969/j.issn.1671-7856.2025.04.003
基于ROS介导NLRP3炎症小体活化探讨凉血退紫方治疗过敏性紫癜大鼠作用机制研究
Mechanism of Liangxue Tuizi Formula in the treatment of Henoch-Schönlein purpura rats via reactive oxygen species-mediated activation of NLRP3 inflammasome
摘要
Abstract
Objective To study the effect of Liangxue Tuizi Formula(LXTZF)on reactive oxygen species(ROS)-mediated NOD-like receptor thermal protein domain associated protein 3(NLRP3)inflammasome activation in Henoch-Schönlein purpura(HSP)rats,and to explore its possible mechanism in the treatment of HSP.Methods Twenty-four rats were divided randomly into four groups:control,model,LXTZF,and compound glycyrrhizin(CG)groups.Except for the control group,a model of HSP was established in the other groups by heat drugs combined with egg albumin.After successful modeling,rats in the LXTZF group were given LXTZF solution 7.47 g/kg,rats in the CG group were given CG solution 13.5 mg/kg by gavage,and rats in the control and model groups were given normal saline solution by gavage once a day for 4 weeks.Samples were collected 8 hours after the last gavage.Skin histopathology changes were observed by hematoxylin and eosin(HE)staining.Serum interleukin(IL)-18 and IL-1βlevels were detected by enzyme-linked immunosorbent assay(ELISA).Changes in ROS levels in the skin were detected by immunofluorescence.Apoptosis-associated speckle-like protein(ASC),NLRP3,cysteinyl aspartate-specific protease-1(Caspase-1)mRNA and protein expression levels in rat skin were detected by real-time quantitative polymerase chain reaction(RT-PCR)and immunohistochemistry and Western blot,respectively.Results The skin pathology in the model group showed obvious inflammatory cell infiltration compared with the control group.Serum IL-18 and IL-1β levels were significantly increased(P＜0.05),skin ROS levels were significantly increased(P＜0.05),and skin ASC,NLRP3,Caspase-1 mRNA and protein expression levels were significantly increased(P＜0.05).Inflammatory cell infiltration in the skin tissues of rats was alleviated in the LXTZF and CG groups compared with the model group,while serum levels of IL-18 and IL-1β were significantly decreased(P＜0.05).ROS levels in the skin were significantly decreased(P＜0.05),and mRNA and protein levels of ASC,NLRP3,and Caspase-1 in the skin were significantly decreased(P＜0.05).Conclusions The mechanism of LXTZF in HSP may be related to the inhibition of ROS-mediated NLRP3 inflammasome activation.关键词
过敏性紫癜/凉血退紫方/ROS/NLRP3炎症小体Key words
Henoch-Schönlein purpura/Liangxue Tuizi Formula/ROS/NLRP3 inflammasome引用本文复制引用
宋金婉,任献青,邢琼琼,李一凡,杨满翔..基于ROS介导NLRP3炎症小体活化探讨凉血退紫方治疗过敏性紫癜大鼠作用机制研究[J].中国比较医学杂志,2025,35(4):21-30,10.基金项目
国家自然科学基金(82374519) （82374519）
河南省省级科技研发计划联合基金项目(222301420022) （222301420022）
2023年度河南省中医学"双一流"创建科学研究专项课题(HSRP-DFCTCM-2023-8-41) （HSRP-DFCTCM-2023-8-41）
河南中医药大学2023年度研究生科研创新类项目(2023KYCX005). （2023KYCX005）
