ArticleCurrent research in neurobiology2026
Sulforaphane enhances locomotor recovery after spinal cord injury through antioxidant, anti-inflammatory, and JAK/STAT-modulating mechanisms.
Article in Current research in neurobiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Spinal cord injury (SCI) leads to irreversible neurological deficits primarily through secondary injury mechanisms, including oxidative stress and glial dysfunction. Sulforaphane (SFN), a naturally occurring isothiocyanate, has shown antioxidant and anti-inflammatory effects in various neurological models, but its impact on Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling and microglial polarization in SCI remains unclear. Adult male Wistar rats were randomly assigned to Sham, SCI, or SCI + SFN groups (n = 10/group). SCI was induced by a moderate T10 contusion, and SFN (50 mg/kg, i.p.) was administered at 10 min, 72 h, and 7 days post-injury. Locomotor recovery was assessed using the Basso-Beattie-Bresnahan (BBB) scale. At day 14, spinal cord tissue was analyzed for oxidative stress markers, including reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD), and reduced glutathione (GSH), as well as JAK2/STAT3 signaling and microglial polarization. SCI significantly increased ROS and MDA levels while reducing SOD activity and GSH content. Phosphorylation of JAK2 and STAT3, along with glial fibrillary acidic protein (GFAP), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6), was markedly elevated. SFN treatment restored antioxidant defenses, suppressed JAK2/STAT3 activation, partially recovered suppressor of cytokine signaling 3 (SOCS3), and reduced pro-inflammatory responses. Moreover, SFN shifted microglial polarization from a pro-inflammatory (M1) toward a reparative (M2) phenotype and significantly improved BBB locomotor scores compared with untreated SCI rats. SFN confers neuroprotection in SCI by reducing oxidative stress, modulating JAK/STAT signaling, rebalancing microglial polarization, and improving locomotor recovery. These findings highlight SFN as a promising candidate for therapeutic development in SCI.
Indexed as
Identifiers
What OpenQuestion holds
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.