Celastrol ameliorates experimental autoimmune neuritis by shifting the polarization of M1/M2 macrophages

被引：0

作者：

Qian, Yun ^{[1
]}

Tang, Bo ^{[1
]}

Jiang, Minhai ^{[1
]}

Lu, Shan ^{[1
]}

Huang, Huan ^{[1
]}

Wei, Wan ^{[1
]}

Yin, Congguo ^{[1
]}

机构：

[1] West Lake Univ, Affiliated Hangzhou Peoples Hosp 1, Sch Med, Dept Neurol, Hangzhou, Peoples R China

来源：

BOLETIN LATINOAMERICANO Y DEL CARIBE DE PLANTAS MEDICINALES Y AROMATICAS | 2025年 / 24卷 / 04期

关键词：

Celastrol; Experimental autoimmune neuritis; Macrophage polarization; NRF2/HIF-1; alpha; Hypoxic responses; GUILLAIN-BARRE-SYNDROME; RECEPTORS; NEUROPROTECTION; CYTOKINES; INJURY; ALPHA; MODEL;

D O I：

10.37360/blacpma.25.24.4.43

中图分类号：

R [医药、卫生];

学科分类号：

10 ;

摘要：

Guillain-Barre syndrome (GBS) is an autoimmune disease with inflammatory infiltration. Macrophage polarization is involved in GBS progression. Celastrol has anti-neuroinflammatory effects, but its mechanism in experimental autoimmune neuritis (EAN) is unclear. We hypothesized that celastrol might shift macrophage polarization via the NRF2/HIF-1 alpha pathway. EAN was induced in male Lewis rats by immunization. Celastrol (1 mg/kg) was administered intragastrically starting from the acute phase onset. Clinical scores, histology, macrophage polarization (flow cytometry and immunofluorescence), cytokines (ELISA), and NRF2/HIF-1 alpha expression (Western blot and immunofluorescence) were assessed. Celastrol significantly reduced EAN severity and neuroinflammation, shifting macrophages from M1 to M2. Pro-inflammatory cytokines decreased, while anti-inflammatory cytokines increased. Celastrol also upregulated NRF2 and downregulated HIF-1 alpha expression. Celastrol may improve EAN by promoting M2 macrophage polarization via the NRF2/HIF-1 alpha pathway, suggesting its potential as a novel therapeutic agent for GBS.

引用

页码：612 / 628

页数：17

共 41 条

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