时珍国医国药2025，Vol.36Issue(23)：4452-4458,7.DOI:10.70976/j.1008-0805.SZGYGY-2025-2307
消斑愈肾方调控Xc-/GPx4/ACSL4/LPCAT3减轻紫癜性肾损伤的机制
The mechanism of Xiaoban Yushen Formula(消斑愈肾方)in alleviating purpuric nephritis injury via regulating system Xc-/GPx4/ACSL4/LPCAT3
摘要
Abstract
Objective To explore the effects of Xiaoban Yushen Formula(消斑愈肾方,XBYSF)on the expression of SLC7A11,p53,ACSL4,LPCAT3,and GPx4 in a rat model of Henoch-Schonlein purpura(HSP)and the related regulatory mechanisms.Methods Eighty SPF-grade SD rats were randomly divided into six groups:the normal control group,model group,Western medicine group,and low/medium/high-dose XBYSF groups.Except for the normal control group,HSP was induced in the other groups by intraperitoneal sen‐sitization and intradermal challenge with ovalbumin(OVA).Model success was confirmed by observing skin purpura formation.After successful modeling,each group received gavage administration at a volume of 1 mL per 100 g body weight once daily.After 21 consecu‐tive days of administration,samples were collected.Renal reactive oxygen species(ROS)content was assessed using DHE staining.The expression levels of the target genes and proteins were detected by Western blot(WB)and quantitative real-time polymerase chain reaction(qRT-PCR),respectively.Results Compared with the normal control group,the model group showed significantly increased renal ROS content,severe renal unit damage,swollen endothelial cells,thickened extracellular matrix,significantly upregulated expres‐sion of p53,ACSL4,and LPCAT3,and significantly downregulated expression of SLC7A11(P<0.01).Compared with the model group,the pathological changes were significantly alleviated,ROS content was reduced,the expression of p53,ACSL4,and LPCAT3 was lower,and the expression of SLC7A11 and GPx4 was higher in all XBYSF groups and the Western medicine group(P<0.01).The pathological changes in the Western medicine group and the medium-dose XBYSF group were similar;however,the levels of the related indicators in the medium-dose XBYSF group were superior to those in the Western medicine group(P<0.05).Conclusion XBYSF can inhibit the expression of ACSL4 and LPCAT3 in the kidneys of HSPN model rats,reducing intracellular lipid peroxidation.It also enhances the expression of SLC7A11 and GPx4,suppresses p53 expression,regulates the GSH/GSSG ratio,reduces excessive ROS accumulation,and alleviates lipid peroxidation.The potential mechanism is that XBYSF regulates intracellular ROS levels,reduces lipid peroxidation,inhibits ferroptosis,alleviates renal involvement,and improves renal function.关键词
铁死亡/过敏性紫癜/紫癜性肾炎/IgA血管炎/脂质过氧化/消斑愈肾方/清润流派Key words
Ferroptosis/Henoch-Schonlein purpura/Purpuric nephritis/IgA vasculitis/Lipid peroxidation/Xiaoban Yushen Formula(消斑愈肾方)/School of clearing and moistening分类
医药卫生引用本文复制引用
刘智慧,张洪鲲,张君,白晓红,王圣治,张少卿,卢晓宇,巩雪,修婵,张帆,孟德雪,杨姝荟..消斑愈肾方调控Xc-/GPx4/ACSL4/LPCAT3减轻紫癜性肾损伤的机制[J].时珍国医国药,2025,36(23):4452-4458,7.基金项目
国家中医药管理局中医药行业科研专项(201507001-03) （201507001-03）
科技部重大新药创制专项(2009ZX103-194) （2009ZX103-194）
国家中医药管理局高水平中医药重点学科建设项目(zyyzdxk-2023036) （zyyzdxk-2023036）
"辽派中医"姚氏儿科学术思想传承与临床创新研究项目(JDZX2015) （JDZX2015）
辽宁省名中医传承工作室项目(辽中医药综合字[2024]19号) （辽中医药综合字[2024]19号）
