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DL-3-n-butylphthalide extends survival by attenuating glial activation in a mouse model of amyotrophic lateral sclerosis
Feng X, Peng Y, Liu M, Cui L.. Neuropharmacology, 2011-11-02
Topic: Brain proteins, microglia and lab models
Amyotrophic lateral sclerosis (ALS) is a lethal neurodegenerative disease characterized by progressive muscular atrophy, paralysis and bulbar symptoms. Transgenic mice over-expressing human mutant Cu/Zn superoxide dismutase-1 (SOD1) mimicked the pathological phenotype of ALS. dl-3-n-butylphthalide (dl-NBP) has been demonstrated to play a neuroprotective role in cerebral ischemia, vascular dementia, and Alzheimer's disease. In the current study, we examined the effect of dl-NBP in Tg (SOD1-G93A) transgenic mice, a well-studied model of ALS. Following the symptomatic onset of disease, oral administration of dl-NBP significantly improved motor performance, extended the survival interval, attenuated motor neuron loss, and delayed motor unit reduction compared to vehicle controls. These observations were further corroborated by the significant reduction in immunoreactivity of CD11b and glial fibrillary acidic protein (GFAP), markers for microglia and astrocytes, respectively. Additionally, downregulation of nuclear factor κB (NF-κB) p65 and tumor necrosis factor-α (TNF-α) protein levels and a slight upregulation of NF-E2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) were found in the spinal cord of Tg (SOD1-G93A) mice treated by dl-NBP. These results suggest that dl-NBP might be a promising compound in the treatment of ALS. This article is part of a Special Issue entitled 'Post-Traumatic Stress Disorder'.
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APA 7th
Feng, X., Peng, Y., Liu, M., & Cui, L. (2012). DL-3-n-butylphthalide extends survival by attenuating glial activation in a mouse model of amyotrophic lateral sclerosis. Neuropharmacology. https://doi.org/10.1016/j.neuropharm.2011.10.009
Vancouver
Feng X, Peng Y, Liu M, Cui L. DL-3-n-butylphthalide extends survival by attenuating glial activation in a mouse model of amyotrophic lateral sclerosis. Neuropharmacology. 2012. doi:10.1016/j.neuropharm.2011.10.009. PMID: 22056419.
BibTeX
@article{feng2012-22056419,
author = {Feng, X. and Peng, Y. and Liu, M. and Cui, L.},
title = {{DL-3-n-butylphthalide extends survival by attenuating glial activation in a mouse model of amyotrophic lateral sclerosis}},
journal = {Neuropharmacology},
year = {2012},
doi = {10.1016/j.neuropharm.2011.10.009},
pmid = {22056419},
url = {https://doi.org/10.1016/j.neuropharm.2011.10.009}
}
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Key findings
- Transgenic mice over-expressing human mutant Cu/Zn superoxide dismutase-1 (SOD1) mimicked the pathological phenotype of ALS. dl-3-n-butylphthalide (dl-NBP) has been demonstrated to play a neuroprotective role in cerebral ischemia, vascular dementia, and Alzheimer's disease.
- Following the symptomatic onset of disease, oral administration of dl-NBP significantly improved motor performance, extended the survival interval, attenuated motor neuron loss, and delayed motor unit reduction compared to vehicle controls.
- These observations were further corroborated by the significant reduction in immunoreactivity of CD11b and glial fibrillary acidic protein (GFAP), markers for microglia and astrocytes, respectively.
- These results suggest that dl-NBP might be a promising compound in the treatment of ALS.
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Study details
- Evidence strengthLow
How this study scored 36/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported and randomised / blinded because the record does not state it. We have no data on journal's citation record, times cited, citations per year, impact for its field and year, cited by studies here, still being cited, senior author's track record, institution's track record and multi-centre collaboration, so those were left out: it earned 21 of the 58 points we could judge it on, which is 36 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Neuropharmacology) |
| Journal's citation record | — / 4 | No journal record from OpenAlex — left out of this score |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 1 / 5 | 2012 — within 20 year(s) of the newest study here |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Laboratory or animal study (title names “mouse”) — scores zero |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | — / 7 | No citation count (not found in OpenAlex) — left out of this score |
| Citations per year | — / 5 | No citation count or no year — left out of this score |
| Impact for its field and year | — / 6 | No field-weighted citation impact (OpenAlex has none yet) — left out of this score |
| Cited by studies here | — / 6 | Not yet checked against this library's citation graph — left out of this score |
| Still being cited | — / 4 | No yearly citation counts — left out of this score |
| Senior author's track record | — / 4 | Senior author's record not available — left out of this score |
| Institution's track record | — / 3 | No institution listed in OpenAlex — left out of this score |
| Multi-centre collaboration | — / 3 | Institutions not listed — left out of this score |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 22056419) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Points | 21 / 58 | Scored on 11 of 20 parts. We have no data for the rest, so they are left out: 21 of the 58 points we could judge it on is 36 out of 100. |
| Total | 36 / 100 | — |
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