Evidence map›Paper›PMID 41206312›Full record

ArticleNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics2026

Salidroside ameliorates experimental autoimmune neuritis by dually modulating neuroinflammation and immune homeostasis via PI3K/AKT signaling.

Tao Gu, Li Wang, Xue Kang, Chunguang Yu, Kaichun Shen, Man Song, Yingying Gao, Guowei Wang, Zhenhai Wang

Abstract read
In one paragraph

Article in Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

Tao GuFirst Clinical Medical College, Ningxia Medical University, Yinchuan, 750004, China.
Li WangFirst Clinical Medical College, Ningxia Medical University, Yinchuan, 750004, China.
Xue KangDepartment of Neurology, Tangdu Hospital, Air Force Military Medical University, Xi'an, 710038, China.
Chunguang YuFirst Clinical Medical College, Ningxia Medical University, Yinchuan, 750004, China.
Kaichun ShenFirst Clinical Medical College, Ningxia Medical University, Yinchuan, 750004, China.
Man SongFirst Clinical Medical College, Ningxia Medical University, Yinchuan, 750004, China.
Yingying GaoFirst Clinical Medical College, Ningxia Medical University, Yinchuan, 750004, China.
Guowei WangNHC Key Laboratory of Diagnosis and Treatment on Brain Functional Diseases, Chongqing, 400016, China; The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China. Electronic address: wangguowei0119@163.com.
Zhenhai WangInstitute of Medical Sciences, General Hospital of Ningxia Medical University, Yinchuan, 750004, China; Diagnosis and Treatment Engineering Technology Research Center of Nervous System Diseases of Ningxia Hui Autonomous Region, Yinchuan, 750004, China; Neurology Center, General Hospital of Ningxia Medical University, Yinchuan, 750004, China. Electronic address: nyfywzh@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Guillain-Barré syndrome (GBS), an acute autoimmune peripheral neuritis, remains a clinical challenge due to limited therapeutic efficacy and heterogeneous patient responses. The present study investigated salidroside (SAL), a bioactive phenylethanoid glycoside derived from Rhodiola rosea, for its dual anti-inflammatory and neuroprotective properties using experimental autoimmune neuritis (EAN), a validated GBS model. Integrated network pharmacology and molecular docking analyses identified PI3K/AKT signaling as the principal mechanistic target of SAL. In vivo administration of SAL (100 ​mg/kg/day, intragastric) significantly reduced neurological deficits, alleviated histopathological damage in sciatic nerves, and restored Th1/Th17-Treg immune balance in EAN rats. Mechanistic analysis demonstrated that SAL inhibited NF-κB activation through inhibition of IκBα degradation and p65 nuclear translocation, leading to downregulation of pro-inflammatory cytokines (TNF-α). Concurrently, SAL promoted macrophage polarization from the pro-inflammatory M1 (CD86

Indexed as

GlucosidesHomeostasisNeuritis, Autoimmune, ExperimentalNeuroinflammatory DiseasesPhenolsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktAnimalsMaleNeuroprotective AgentsRatsRats, Inbred LewSignal TransductionGlucosidesNeuroprotective AgentsPhenolsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktrhodiolosideImmune homeostasisMacrophage polarizationNeuroinflammationPI3K/AKT signalingSalidroside

Identifiers

PMID41206312
PMCPMC12976540

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.