ArticleJournal of molecular histology2026
Dendrobium officinale polysaccharides alleviate atopic dermatitis in vivo and in vitro through inhibition of inflammation and mitochondrial dysfunction.
Article in Journal of molecular histology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
Abstract
Atopic dermatitis (AD) is a chronic inflammatory skin disorder marked by immune dysregulation and oxidative stress. Current therapies, such as corticosteroids, have side effects, necessitating new treatments. This study investigates the therapeutic effects of Dendrobium officinale polysaccharides (DOP) on AD, specifically focusing on their role in modulating inflammation and mitochondrial dysfunction. An AD-like model was induced in BALB/c mice, while HaCaT keratinocytes stimulated with TNF-α/IFN-γ served as an in vitro model. In mice, DOP significantly alleviated AD symptoms, reduced inflammatory cytokines (IL-1β, IL-6) and oxidative stress markers (MDA, NO), and restored antioxidant enzyme levels (GSH, SOD, CAT). In HaCaT cells, DOP ameliorated mitochondrial dysfunction, evident by increased mitochondrial membrane potential, cellular ATP content, and normalized mitochondrial dynamics (restoring MFN1/MFN2 and reducing DRP1). Furthermore, DOP suppressed NF-κB activation both in vivo and in vitro. These findings suggest that DOP alleviates AD by reducing inflammation and oxidative stress while preserving mitochondrial homeostasis. The mechanism appears associated with NF-κB inhibition, though this link is correlational and requires further direct validation.
Indexed as
Identifiers
41886005What 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.