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五子衍宗丸通过甲酰肽受体2通路抑制神经炎症OACHSSCD

Wuzi Yanzong Pills Inhibit Neuroinflammation via the Formyl Peptide Receptor 2 Pathway

中文摘要英文摘要

目的:探讨五子衍宗丸(WYP)对1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)诱导的小鼠神经炎症的影响,以及对甲酰基肽受体2(FPR2)-小鼠消退素D1(RvD1)/p38促分裂原活化的蛋白激酶(p38 MAPK)/核因子κB(NF-κB)通路的调控作用.方法:60只小鼠随机分为对照组(Con)、MPTP组、WYP组、阳性药组(L-DOPA)组,对小鼠行为学进行测定;免疫荧光法检测小鼠脑组织酪氨酸羟化酶(TH)、FPR2、离子钙结合衔接分子1(Iba1)和NF-κB;酶联免疫吸附试验(ELISA)检测小鼠脑组织匀浆FPR2、RvD1、肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)以及白细胞介素-1β(IL-1β)水平;实时荧光定量逆转录聚合酶链反应(qRT-PCR)检测FPR2、Iba1和p38 mRNA水平;蛋白质印迹法(WB)检测TH和FPR2的表达.结果:与Con组比较,MPTP小鼠运动协调性降低,脑组织FPR2、TNF-α、IL-6、IL-1β、Iba1、p38以及NF-κB表达增加(P<0.05),TH和RvD1表达降低(P<0.05);与MPTP组比较,WYP组小鼠运动协调能力改善、脑组织TNF-α、IL-6、IL-1β、Iba1、p38以及NF-κB表达降低(P<0.05),TH表达升高(P<0.05),而FPR2相较于MPTP组增加更为显著,但研究发现FPR2的配体RvD1显著增加.结论:WYP通过影响FPR2和RvD1特异性结合,干预p38 MAPK/NF-κB信号通路抑制MPTP诱导的小鼠神经炎症.

Objective:To investigate the effects of Wuzi Yanzong Pills(WYP)on MPTP-induced neuroinflammation in mice and explore its regulatory role in the formyl peptide receptor 2(FPR2)-resolvin D1(RvD1)/p38 mitogen-activated protein kinase(p38 MAPK)/nuclear factor κB(NF-κB)signaling pathway.Methods:Sixty mice were randomly assigned to four groups:control(Con),MPTP,WYP,and positive control(L-DOPA).Behavioral assessments were performed to evaluate motor coordination.Immunofluo-rescence(IF)was used to detect tyrosine hydroxylase(TH),FPR2,ionized calcium-binding adapter molecule 1(Iba1),and NF-κB in brain tissue.Levels of FPR2,RvD1,tumor necrosis factor-α(TNF-α),interleukin-6(IL-6),and interleukin-1 β(IL-1β)in brain homogenates were measured using enzyme-linked immunosorbent assay(ELISA).Quantitative real-time PCR(qRT-PCR)assessed mRNA expression of FPR2,Iba1,and p38,while Western blot(WB)analyzed protein expression of TH and FPR2.Results:Com-pared with the Con group,MPTP-treated mice showed impaired motor coordination,increased expression of FPR2,TNF-α,IL-6,IL-1 β,Iba1,p38,and NF-κB in brain tissue(P<0.05),and decreased expression of TH and RvD1(P<0.05).Compared with the MPTP group,WYP treatment improved motor coordination,decreased TNF-α,IL-6,IL-1 β,Iba1,p38,and NF-κB expression(P<0.05),and increased TH expression(P<0.05).Notably,FPR2 expression was further elevated in the WYP group compared to the MPTP group,accompanied by a significant increase in its ligand,RvD 1.Conclusion:WYP inhibits MPTP-induced neuroinflamma-tion in mice by enhancing the specific interaction between FPR2 and RvD1,thereby modulating the p38 MAPK/NF-κB signaling pathway.

徐磊;冯子淇;李志新;胡敏;樊慧杰;柴智

山西中医药大学多发性硬化益气活血重点研究室/神经生物学研究中心,晋中,030619山西中医药大学多发性硬化益气活血重点研究室/神经生物学研究中心,晋中,030619山西中医药大学多发性硬化益气活血重点研究室/神经生物学研究中心,晋中,030619山西中医药大学多发性硬化益气活血重点研究室/神经生物学研究中心,晋中,030619山西中医药大学多发性硬化益气活血重点研究室/神经生物学研究中心,晋中,030619山西中医药大学多发性硬化益气活血重点研究室/神经生物学研究中心,晋中,030619

医药卫生

五子衍宗丸帕金森病神经炎症甲酰肽受体2消退素D1p38促分裂原活化的蛋白激酶核因子κB信号通路

Wuzi Yanzong PillsParkinson's diseaseNeuroinflammationFormyl peptide receptor 2Resolvin DIP38 mito-gen-activated protein kinaseNuclear factor-kappa BSignaling pathway

《世界中医药》 2026 (5)

822-828,7

国家自然科学基金项目(82574609)国家中医药管理局青年岐黄学者培养项目(国中医药人教函[2022]256号)山西省基础研究计划青年科学研究项目(202203021222279).

10.3969/j.issn.1673-7202.2026.05.010

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