ArticleMolecular neurobiology2025
Mogroside V Ameliorates Spinal Cord Injury by Inhibiting M1 Microglia Polarization.
Article in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
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Who cites it
2 citing papers in PubMed.
- Every-Other-Day Fasting Prehabilitation Attenuates Secondary Injury Following Spinal Cord Injury and Is Associated with Stage-Dependent SREBP1-Related Metabolic-Immune Remodeling.Molecular neurobiology · 2026Article
- Modulatory effects of traditional Chinese medicine and derived active metabolites on autoimmune-inflammatory signaling pathways in multiple sclerosis: a narrative review.Frontiers in pharmacology · 2026Review
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
Spinal cord injury (SCI) constitutes a severe disorder of the central nervous system that is usually caused by external traumatic forces that damage the spinal cord's structure and disrupt its normal functions. SCI is characterized by a high disability rate and limited treatment options. The current treatments include surgery, medication, and rehabilitation. Additionally, some traditional Chinese medicines and their ingredients have shown potential effects in the treatment of SCI. Mogroside-V (Mog-V), derived from Siraitia grosvenorii, displays a range of biological functions, such as anti-inflammatory effects, antitumor actions, and antioxidant potential. However, the effect and fundamental mechanism of Mog-V on SCI remain unclear. In this study, we established a spinal cord contusion model in C57BL/6 mice to evaluate the effects of Mog-V. The results revealed that Mog-V effectively improved lower limb motor function after SCI in mice. Mog-V inhibited pro-inflammatory macrophage/microglia polarization in vivo and reduced the secretion levels of macrophage/microglia-associated pro-inflammatory cytokines, including interleukin (IL)-12, IL-6, IL-1β, and tumor necrosis factor-α (TNF-α). Mog-V effectively inhibited M1 microglial polarization and the release of their associated pro-inflammatory cytokines in vitro. Mog-V also inhibited the phosphorylation of P65, P38, JNK, and ERK proteins in vitro and P38, JNK, and ERK proteins in vivo. Overall, Mog-V may improve SCI by inhibiting M1 microglia/pro-inflammatory macrophage polarization and reducing the release of inflammatory cytokines via the mitogen-activated protein kinase (MAPK) and NF-κB signaling pathways, highlighting the potential use of Mog-V for SCI treatment.
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Registered trials
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