ArticleCell death discovery2024
Salidroside promotes the repair of spinal cord injury by inhibiting astrocyte polarization, promoting neural stem cell proliferation and neuronal differentiation.
Article in Cell death discovery, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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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.
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.
Who cites it
13 citing papers in PubMed.
- Natural Products and Neuroregeneration: Rethinking Discovery Beyond Bioavailability Through Pseudo-Natural Product Design.Biomedicines · 2026Review
- Delta-opioid receptor-mediated neural protection and regeneration.Neural regeneration research · 2026Article
- Targeting the fibrosis-inflammation-oxidative stress axis: multifaceted mechanisms of salidroside in chronic organ fibrosis.Apoptosis : an international journal on programmed cell death · 2026Review
- STAT3 Signaling in Spinal Cord Injury: Neurochemical Mechanisms Linking Neuroinflammation, Mitochondrial Stress, and Glial Remodeling.Neurochemical research · 2026Review
- Hypoxia Upregulates RIPK1 via the HIF-1α-JAK-STAT Pathway Leading to Astrocyte Necroptosis to Promote Cavitation After Spinal Cord Injury.CNS neuroscience & therapeutics · 2026Article
- Reprogramming the Inflammatory Response to Promote Neural Stem Cell Function After Spinal Cord Injury.Molecular neurobiology · 2026Review
- The hippocampal subgranular zone neurogenic niche: a modular perspective on neural stem cell regulation.Frontiers in cellular neuroscience · 2026Review
- Repurposing of Chemokine Antagonists for Combined Phase-Resolved Spinal Cord Injury Treatment.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Salidroside-Pretreated Small Extracellular Vesicles Derived from Human Umbilical Cord Mesenchymal Stem Cells Promote Blood-Spinal Cord Barrier Repair After Spinal Cord Injury in Mice.Molecular neurobiology · 2025Article
- Precision Recovery After Spinal Cord Injury: Integrating CRISPR Technologies, AI-Driven Therapeutics, Single-Cell Omics, and System Neuroregeneration.International journal of molecular sciences · 2025Review
- [Effect of removing microglia from spinal cord on nerve repair after spinal cord injury in mice].Zhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery · 2025Article
- Bioactive compounds from Chinese herbal plants for neurological health: mechanisms, pathways, and functional food applications.Frontiers in nutrition · 2025Review
- Targeting astrocytes polarization after spinal cord injury: a promising direction.Frontiers in cellular neuroscience · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
Spinal cord injury (SCI) remains a formidable challenge, lacking effective treatments. Following SCI, neural stem cells (NSCs) migrate to SCI sites, offering a potential avenue for nerve regeneration, but the effectiveness of this intrinsic repair mechanism remains suboptimal. Salidroside has demonstrated pro-repair attributes in various pathological conditions, including arthritis and cerebral ischemia, and the ability to curtail early-stage inflammation following SCI. However, the specific role of salidroside in the late-stage repair processes of SCI remains less defined. In this investigation, we observed that continuous salidroside treatment in SCI mice improved motor function recovery. Immunofluorescence-staining corroborated salidroside's capacity to stimulate nerve regeneration and remyelination, suppress glial scar hyperplasia, reduce the activation of neurotoxic A1 astrocytes, and facilitate NSCs migration towards the injured region. Mechanistically, in vitro experiments elucidated salidroside's significant role in restraining astrocyte proliferation and A1 polarization. It was further established that A1 astrocytes hinder NSCs proliferation while inducing their differentiation into astrocytes. Salidroside effectively ameliorated this inhibition of NSCs proliferation through diminishing c-Jun N-terminal kinase (JNK) pathway phosphorylation and restored their differentiation into neurons by suppressing the signal transducer and activator of transcription 3 (STAT3) pathway. In summary, our findings suggest that salidroside holds promise as a therapeutic agent for traumatic SCI treatment.
Identifiers
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Registered trials
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.