Key Takeaways & Executive Findings
- •• Tanshinones from Salvia miltiorrhiza alleviate DSS-induced ulcerative colitis by reducing inflammation and restoring intestinal barrier integrity. • Integrated multi-omics reveals that tanshinones reprogram the gut microbiota-metabolite axis, reversing dysbiosis and correcting metabolic disturbances. • Key microbial modules link beneficial bacteria like Akkermansia to anti-inflammatory lipid mediators, while pathobionts like Desulfovibrio are associated with disrupted bile acid metabolism. • Supplementation with Akkermansia muciniphila synergizes with tanshinone IIA to enhance barrier restoration and metabolic normalization, highlighting microbiome-targeting therapeutic potential.
Abstract
The anti-inflammatory properties of the traditional herb Salvia miltiorrhiza Bunge are well-established, yet its precise mechanism of action in ulcerative colitis (UC) remains unclear. Herein, we evaluate the therapeutic potential of four major tanshinones–tanshinone IIA (Tan IIA), miltirone, neocryptotanshinone, and dihydrotanshinone I–in a murine dextran sulfate sodium (DSS)-induced colitis model. Our results show that tanshinones effectively alleviate disease severity, suppress systemic and local inflammation, and restore intestinal barrier integrity. Integrated multi-omics analysis reveals that the therapeutic efficacy originates from a comprehensive reprogramming of the gut microbiota-metabolite axis. Specifically, tanshinones reverse colitis-associated dysbiosis and rectify metabolic disturbances in linoleic acid metabolism, bile acid biosynthesis, and amino acid utilization. Correlation network analysis identifies key functional modules linking beneficial microbes (e.g., Akkermansia) to anti-inflammatory lipid mediators and associating pathobionts (e.g., Desulfovibrio) with disrupted bile acid metabolism. Notably, supplementation with Akkermansia muciniphila synergizes with Tan IIA to amplify barrier restoration and metabolic normalization. Our findings establish that tanshinones ameliorate UC through microbiota-driven metabolic reprogramming, wherein the restructured microbial community actively shapes a therapeutic metabolic output. This work elucidates a metabolite-mediated mechanism of action and positions tanshinones as promising microbiome-targeting therapeutics for inflammatory bowel disease.
1. Introduction
Ulcerative colitis (UC) is a chronic and relapsing inflammatory bowel disease (IBD) characterized by abdominal pain, bloody diarrhea, and weight loss [1,2]. While biological therapies targeting pro-inflammatory cytokines have revolutionized treatment, their variable efficacy and secondary failure highlight an urgent need for novel therapeutic strategies [3,4].
The pathogenesis of UC involves a complex interplay of genetic susceptibility, immune dysregulation, and environmental factors [5–7]. Among these, dysbiosis of the gut microbiota is recognized as a pivotal contributor [7,8]. Patients with UC exhibit a distinct loss of microbial diversity, an expansion of pro-inflammatory pathobionts (e.g., Proteobacteria and Enterobacteriaceae), and a reduction in beneficial commensals (e.g., Adlercreutzia) [9–12]. Importantly, gut dysbiosis in UC leads to a profound reprogramming of the gut metabolome, characterized by disrupted production of key metabolites such as short-chain fatty acids (SCFAs), bile acids (BAs), and tryptophan derivatives [8,12–14]. These metabolic alterations are not merely bystanders but active drivers of intestinal inflammation, barrier dysfunction, and immune imbalance [15]. Consequently, therapeutic strategies capable of restoring microbial ecological balance and metabolic homeostasis represent a promising avenue for UC intervention.
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Zhe Liu, Chan Hui, Guochao Zhang, Haicheng Yang, Yi Wang, Yaqian Shi, Chao Wang, Yanfei Liu, Xia Gao, Yuting Wen (2026). Tanshinones from Salvia miltiorrhiza alleviate ulcerative colitis via reprogramming the gut microbiota-metabolite axis. Acta Biochimica et Biophysica Sinica. https://doi.org/10.3724/abbs.2026054
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Frequently Asked Questions
What are the main findings of this study on tanshinones and ulcerative colitis?
The study demonstrates that four major tanshinones from Salvia miltiorrhiza alleviate DSS-induced ulcerative colitis in mice by reducing inflammation, restoring intestinal barrier integrity, and reprogramming the gut microbiota-metabolite axis. Specifically, they reverse dysbiosis and correct metabolic disturbances in linoleic acid, bile acid, and amino acid metabolism, with key microbial modules linking beneficial bacteria like Akkermansia to anti-inflammatory lipid mediators.
How do tanshinones exert their therapeutic effects in ulcerative colitis?
Tanshinones exert their effects through microbiota-driven metabolic reprogramming. They reshape the gut microbial community, promoting beneficial microbes such as Akkermansia and suppressing pathobionts like Desulfovibrio, which in turn leads to the production of anti-inflammatory metabolites and restoration of metabolic homeostasis, thereby ameliorating colitis.
What is the significance of Akkermansia muciniphila in this study?
Akkermansia muciniphila was identified as a key beneficial microbe associated with anti-inflammatory lipid mediators. Supplementation with A. muciniphila synergized with tanshinone IIA to amplify barrier restoration and metabolic normalization, suggesting that targeting this microbe could enhance the therapeutic efficacy of tanshinones.
What experimental model was used to evaluate the effects of tanshinones?
The study used a murine dextran sulfate sodium (DSS)-induced colitis model, a widely accepted experimental model for ulcerative colitis. Mice were treated with tanshinones or sulfasalazine (positive control), and disease severity, inflammation, barrier integrity, and multi-omics profiles were assessed.
What are the potential clinical implications of this research?
The findings position tanshinones as promising microbiome-targeting therapeutics for inflammatory bowel disease. By elucidating the metabolite-mediated mechanism of action, this research supports the development of tanshinone-based therapies that could modulate the gut microbiota and metabolic pathways to treat UC, potentially offering an alternative or adjunct to current biological therapies.
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