ArticleChinese medicine2026
Xiao Chai Hu Decoction ameliorates doxorubicin-induced cardiotoxicity through an Akkermansia muciniphila-associated gut-heart mechanism.
Article in Chinese medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundDoxorubicin (DOX) induces cardiotoxicity partly through ferroptosis. Xiao Chai Hu Decoction (XCHD) has anti-inflammatory and organ-protective activities, but its effects on DOX-induced cardiac injury and the gut-heart axis remain unclear. PURPOSE: This study investigated whether XCHD attenuates DOX-induced cardiotoxicity through gut microbiota remodeling, with particular emphasis on the contribution of Akkermansia muciniphila and the downstream involvement of BMP10-associated ferroptosis.
methodsMale C57BL/6 mice received DOX (5 mg/kg/week for 4 weeks; cumulative dose, 20 mg/kg) and XCHD (5-20 g/kg/day). Cardiac function, myocardial injury, histopathology, iron accumulation, and ferroptosis-related indices were evaluated. Cardiac transcriptomics and fecal 16S rRNA sequencing were combined with antibiotic-mediated microbiota depletion, fecal microbiota transplantation (FMT), and A. muciniphila supplementation to assess microbiota involvement. H9c2 cells treated with XCHD-containing serum and subjected to BMP10 knockdown were used to examine the downstream role of BMP10.
resultsXCHD improved cardiac function and reduced myocardial injury, fibrosis, iron accumulation, and ferroptosis-associated alterations. Transcriptomic analysis identified BMP10 as a candidate downstream factor suppressed by DOX and restored by XCHD. In H9c2 cells, XCHD-containing serum attenuated ferroptosis-associated changes, whereas BMP10 knockdown weakened these effects, supporting a functional contribution of BMP10 in vitro. XCHD also preserved intestinal barrier integrity, reshaped the gut microbiota, and enriched A. muciniphila. Microbiota depletion abolished the protective effects of XCHD, whereas FMT transferred the protective phenotype. A. muciniphila supplementation reproduced key cardiac and anti-ferroptotic effects, with live bacteria producing greater benefits than heat-inactivated bacteria; these changes were accompanied by restoration of myocardial BMP10 expression.
conclusionXCHD alleviates DOX-induced cardiotoxicity through an A. muciniphila-associated, microbiota-dependent gut-heart mechanism involving intestinal barrier preservation and attenuation of ferroptosis-associated injury. These findings support a "TCM formula-gut microbiota-host response-regulated cell death" framework for XCHD-mediated cardioprotection.
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