ArticleJournal of cellular and molecular medicine2017
Dl-3-n-butylphthalide attenuates acute inflammatory activation in rats with spinal cord injury by inhibiting microglial TLR4/NF-κB signalling.
Article in Journal of cellular and molecular medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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
28 citing papers in PubMed, 44 citations in OpenAlex.
- Plant-derived therapies in Parkinson's disease: a systematic review of clinical evidence.Journal of neural transmission (Vienna, Austria : 1996) · 2026Review
- The Impact of Nuclear Factor Kappa B on the Response of Microglia in Spinal Cord Injuries.Cureus · 2025Review
- DIA-based proteomics reveals anti-inflammatory role of DL-3-Translational neuroscience · 2025Article
- MSR405: Inhibiting Neuroinflammation after Spinal Cord Injury in Rats.Biomedicines · 2024Article
- Review
- Neurological Applications of Celery (Molecules (Basel, Switzerland) · 2023Article
- Co-administration of Nanowired DL-3-n-Butylphthalide (DL-NBP) Together with Mesenchymal Stem Cells, Monoclonal Antibodies to Alpha Synuclein and TDP-43 (TAR DNA-Binding Protein 43) Enhance Superior Neuroprotection in Parkinson's Disease Following Concussive Head Injury.Advances in neurobiology · 2023Review
- DI-3-n-butylphthalide mitigates stress-induced cognitive deficits in mice through inhibition of NLRP3-Mediated neuroinflammation.Neurobiology of stress · 2022Article
- Reveal the Antimigraine Mechanism of Chuanxiong Rhizoma and Cyperi Rhizoma Based on the Integrated Analysis of Metabolomics and Network Pharmacology.Frontiers in pharmacology · 2022Article
- Role of Butylphthalide in Immunity and Inflammation: Butylphthalide May Be a Potential Therapy for Anti-Inflammation and Immunoregulation.Oxidative medicine and cellular longevity · 2022Review
- Dl-3-n-Butylphthalide Improves Neuroinflammation in Mice with Repeated Cerebral Ischemia-Reperfusion Injury through the Nrf2-Mediated Antioxidant Response and TLR4/MyD88/NF-Oxidative medicine and cellular longevity · 2022Article
- The PI3K/AKT Pathway-The Potential Key Mechanisms of Traditional Chinese Medicine for Stroke.Frontiers in medicine · 2022Review
- Dl-3-n-Butylphthalide (NBP) Mitigates Muscular Injury Induced by Limb Ischemia/Reperfusion in Mice through the HMGB1/TLR4/NF-Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Vascular protection and regenerative effects of intranasal DL-3-N-butylphthalide treatment after ischaemic stroke in mice.Stroke and vascular neurology · 2021Article
- Total flavonoids of hawthorn leaves promote motor function recovery via inhibition of apoptosis after spinal cord injury.Neural regeneration research · 2021Article
- Neuroinflammation and Modulation Role of Natural Products After Spinal Cord Injury.Journal of inflammation research · 2021Review
- TLR4 promotes microglial pyroptosis via lncRNA-F630028O10Rik by activating PI3K/AKT pathway after spinal cord injury.Cell death & disease · 2020Article
- Curcumin protects BV2 cells against lipopolysaccharide-induced injury via adjusting the miR-362-3p/TLR4 axis.Molecular biology reports · 2020Article
- Dl-3n-butylphthalide improves spatial learning and memory in rats with vascular dementia by reducing autophagy via regulation of the mTOR signaling pathway.Experimental and therapeutic medicine · 2020Article
- Suppressors of cytokine signalling (SOCS)-1 inhibits neuroinflammation by regulating ROS and TLR4 in BV2 cells.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors at 3 institutions in 2 countries.
Funding
Abstract
In this study, we examined the neuroprotective effects and anti-inflammatory properties of Dl-3-n-butylphthalide (NBP) in Sprague-Dawley (SD) rats following traumatic spinal cord injury (SCI) as well as microglia activation and inflammatory response both in vivo and in vitro. Our results showed that NBP improved the locomotor recovery of SD rats after SCI an significantly diminished the lesion cavity area of the spinal cord, apoptotic activity in neurons, and the number of TUNEL-positive cells at 7 days post-injury. NBP inhibited activation of microglia, diminished the release of inflammatory mediators, and reduced the upregulation of microglial TLR4/NF-κB expression at 1 day post-injury. In a co-culture system with BV-2 cells and PC12 cells, NBP significantly reduced the cytotoxicity of BV-2 cells following lipopolysaccharide (LPS) stimulation. In addition, NBP reduced the activation of BV-2 cells, diminished the release of inflammatory mediators, and inhibited microglial TLR4/NF-κB expression in BV-2 cells. Our findings demonstrate that NBP may have neuroprotective and anti-inflammatory properties in the treatment of SCI by inhibiting the activation of microglia via TLR4/NF-κB signalling.
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.