ArticleScientific reports2026
Peiminine attenuates inflammatory bowel disease by suppressing TLR4 mediated NFƙB pathway: an integrated network pharmacology and experimental validation.
Article in Scientific reports, 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
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ulcerative colitis and Crohn’s disease are two of the complex and recurring inflammatory conditions that comprise inflammatory bowel disease. There are currently relatively few therapeutic alternatives available for its treatment, and those that are available have serious side effects. It is also in a very progressive and prevalent phase. Therefore, it is necessary to find safer and more effective therapeutics for its treatment. Targeting different molecular pathways, peiminine has antioxidant and anti-inflammatory qualities. Integrated network pharmacology and molecular docking depicted various targets, amongst them NFƙB and TNF-α were the targets where peiminine elicited maximum binding affinity. Validating the in silico data, further in in vivo study, mice were randomly allocated into six groups: Normal control (NC), Disease control (DC-TNBS, 2,4,6-trinitrobenzene sulfonic acid), STD (TNBS + sulfasalazine 100 mg/kg, p.o.), PEI1, PEI2 & PEI3 (TNBS + Peiminine 1, 2.5, & 5 mg/kg, p.o.), respectively. A sharp fall in disease activity index (DAI) and changes in histopathological examination revealed the colonoprotective effect of peiminine. It also depicted anti-oxidant activity through reducing the levels of myeloperoxidase (MPO) and nitric oxide (NO) and elevating superoxide dismutase (SOD), and catalase (CAT). It downregulated various pro-inflammatory mediators such as tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) in in vitro and in vivo studies, depicting its anti-inflammatory activity. Peiminine has also been shown to have strong anti-inflammatory properties by downregulating the gene expression of TLR4 (1.96-fold), NFƙB (1.70-fold), iNOS (1.27-fold), COX-2 (2.40-fold), and IL-1β (0.80-fold). Meanwhile, it increases the expression of anti-inflammatory mediator IL-10 (2.55-fold). Collectively, peiminine likely decreased colon damage and TNBS-induced colitis through the TLR4-mediated NFƙB pathway.
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.