ArticleGut microbes
Gut microbiota-mediated C-sulfonate metabolism impairs the bioavailability and anti-cholestatic efficacy of andrographolide.
Article in Gut microbes. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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.
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Who cites it
5 citing papers in PubMed.
- Comprehensively investigating pharmacokinetics and metabolic fate of andrographolide in rats by liquid chromatography/mass spectrometry-based approach.RSC advances · 2026Article
- Transcriptional insights into aflatoxin B1 induced hepatotoxicity and comparative effects of medicinal herbs in pigs.BMC veterinary research · 2026Article
- Article
- Andrographolide and Its Derivatives: A Comprehensive Review of Anti-Infective Properties and Clinical Potential.Molecules (Basel, Switzerland) · 2025Review
- Gut microbiome and inflammation in cardiovascular drug response: trends in therapeutic success and commercial focus.Inflammopharmacology · 2025Review
Corrections and comments
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cholestatic liver injury results from the accumulation of toxic bile acids in the liver, presenting a therapeutic challenge with no effective treatment available to date. Andrographolide (AP) has exhibited potential as a treatment for cholestatic liver disease. However, its limited oral bioavailability poses a significant obstacle to harnessing its potent therapeutic properties and restricts its clinical utility. This limitation is potentially attributed to the involvement of gut microbiota in AP metabolism. In our study, employing pseudo-germ-free, germ-free and strain colonization animal models, along with 16S rRNA and shotgun metagenomic sequencing analysis, we elucidate the pivotal role played by gut microbiota in the C-sulfonate metabolism of AP, a process profoundly affecting its bioavailability and anti-cholestatic efficacy. Subsequent investigations pinpoint a specific enzyme, adenosine-5'-phosphosulfate (APS) reductase, predominantly produced by
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