ArticleFrontiers in pharmacology2026
Intestinal toxicity evaluation of polygala total saponins in mice according to toxicological evidence chain (TEC) concept.
Article in Frontiers in pharmacology, 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
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Polygalae Radix a widely used tranquilizing traditional Chinese medicine, is limited by gastrointestinal adverse effects. The Polygala total saponins are identified as its major toxic constituents. Methods: To clarify the toxicity of PTS and elucidate its underlying toxic mechanism, this study performed five key experiments: First, we observed the toxic manifestations of PTS in male ICR mice and collected serum and intestinal tissue samples after administration. Second, we obtained toxicological evidence through histopathological examination and serum biochemical analysis. Third, we detected the protein and mRNA expression levels of tight junctions (TJs) in intestinal tissues, as well as the content of short-chain fatty acids (SCFAs) in feces. Fourth, we analyzed fecal microbial community structure using 16S rRNA gene sequencing after PTS exposure. Fifth, we explored the potential toxic mechanisms using metabolomics and transcriptomic analysis. Results: Three days after PTS administration (i.g., 120 and 240 mg/kg/d), mice exhibited obvious intestinal damage. The main mechanisms underlying PTS-induced intestinal toxicity involved disrupted digestive and absorptive functions, enhanced intestinal inflammation, impaired intestinal barrier integrity (including compromised tight junctions), and severe intestinal microbiota dysbiosis. Notably, intestinal microbiota dysbiosis was closely correlated with body weight loss and intestinal barrier injury in PTS-treated mice. Further analysis revealed that PTS significantly reduced the abundance of multiple genera within the Lachnospiraceae family and tended to decrease short-chain fatty acid (SCFA) levels. Mechanistically, PTS promoted intestinal inflammation at least partially by upregulating arachidonic acid metabolism. Conclusion: This study interprets the mechanism of intestinal toxicity of PTS from the perspectives of metabolites, DEGs, and microbiota. This helps us refine the toxicological evidence chain (TEC) of PTS and further understand its toxicity mechanism.
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.