ArticleImmunity, inflammation and disease2026
Reducing Neuroinflammation via Inhibition of Fibrinogen Deposition and Microglial Activation as an Underlying Mechanism of Paning I Decoction in Ameliorating Parkinson's Disease Symptoms.
Article in Immunity, inflammation and disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Hematological Inflammatory Indices and Coagulation Parameters in Individuals with Substance Use Disorder: A Comparative Study with Healthy Controls.Biomedicines · 2026Article
- Reducing Neuroinflammation via Inhibition of Fibrinogen Deposition and Microglial Activation as an Underlying Mechanism of Paning I Decoction in Ameliorating Parkinson's Disease Symptoms.Immunity, inflammation and disease · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
backgroundParkinson's disease (PD) is a major neurodegenerative disorder. Some patients show limited response to standard therapies, driving the need for new complementary treatments. Paning I decoction (PNID), a traditional herbal formula, has shown the potential to alleviate PD symptoms, but its exact mechanisms remain unclear.
methodsWe tested PNID in a mouse model of PD induced by a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Mice received different PNID doses to evaluate symptom alleviation. We used behavioral tests and laboratory analyses to study brain changes, including neuron damage assessment, dopamine and tyrosine hydroxylase (TH) measurements, blood-brain barrier (BBB) integrity and microglia evaluation, and inflammatory marker analysis.
resultsPNID treatment alleviated PD symptoms in a dose-dependent manner. High-dose PNID performed similarly to Madopar. Neuron protection: increased dopamine and TH expression. BBB repair: less leakage and fibrinogen accumulation. Regulation of polarization: shifted microglia from M1 to M2 states. Inflammation control: lowered pro-inflammatory factors (IL-6, IL-1β, and TNF-α) while increasing anti-inflammatory factors (IFN-β, IL-10, and IL-4).
conclusionsPNID may serve as a promising complementary therapy for PD. Benefits may come from the repair of the BBB, reduction of fibrinogen deposition, and decline in neuroinflammation by modulating microglial polarization.
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.