ArticleInflammopharmacology2026
Yucca filamentosa extract therapeutic potential against neuro-inflammation and demyelination through modulation of eicosanoids.
Article in Inflammopharmacology, 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
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMultiple sclerosis is a chronic inflammatory disease characterized by the demyelination of nerve cells. So, it is mandatory to find out such phytochemicals that may prove to be helpful in treating neurodegeneration. Yucca filamentosa possesses anti-inflammatory, antioxidant and healing properties for the damaged neurons.
methodYucca filamentosa extract (YFE) was prepared and GCMS fingerprinting and molecular docking was performed. Animals divided as Normal, Demyelination disease model, Standard care group, and three treatment groups as YFE 250 mg/kg, 500 mg/kg and 750 mg/kg. Cuprizone 0.2% was mixed in chow diet to induce multiple sclerosis for 42 days.
resultsGC-MS profiling indicates the presence of oleic acid, phytol, and thymol. Neurobehavioral studies were carried out after YFE treatment. Cuprizone caused motor dysfunction as well as anxiety-like behavior in rats. Treatment groups showed notable improvement in the function of motor neurons, and cognition in behavioral tests. YFE downregulated mRNA expression of TNFα, IL-6, ABPP, Alpha synuclein, and acetylcholinesterase. YFE also decreased serum level of TNF-α, IL-6, PGE
conclusionYFE exhibited neuroprotective potential through inhibition of oxidative stress, inflammation and modulation of neurodegenerative markers.
Indexed as
Identifiers
42680956What Socratic 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 Socratic graph.