Frontiers in pharmacology · 2026
Gut microbiota-derived butyrate contributes to baicalin-induced attenuation of hypertensive vascular remodeling via adventitial immunity.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Xie Qiurong, Yang Yanyan, Lin Jiekun, Ye Yuehong, Lin Jiyan, Wu Meizhu, Guo Zhi, Shen Aling, Zeng Weiquan, Peng Jun
Аннотация
BACKGROUND: Baicalin shows potent vasculoprotective effects against hypertension despite poor oral bioavailability. We investigated whether gut microbiota modulation contributes to the systemic vasculoprotective effects of orally administered baicalin.
METHODS: We utilized an Angiotensin II-induced hypertensive mouse model, employing broad-spectrum antibiotics, 16S rRNA sequencing, metabolomics, and in vitro co-culture assays to map the gut-immune-vascular axis.
RESULTS: Oral Baicalin significantly attenuated Ang II-induced blood pressure elevation and improved the intestinal barrier integrity. Antibiotic-induced microbiota depletion substantially weakened these protective effects, supporting a major microbiota contribution under the present experimental conditions. Baicalin reshaped the gut microbial community, enriched SCFA-supporting taxa, and restored a putative butyrate-associated microbial signature, enriching Akkermansia and Lactobacillus accompanied by increased cecal butyrate levels. Exogenous sodium butyrate recapitulated several major protective features of Baicalin treatment, including expansion of Foxp3+ regulatory T cells in mesenteric lymph nodes. These immune changes were accompanied by increased Foxp3+ regulatory immune-cell accumulation in the aortic adventitia. In vitro, butyrate-licensed Tregs suppressed Ang II-induced vascular smooth muscle cell (VSMC) proliferative responses, at least partly through IL-10-mediated inhibition of MAPK/ERK signalling.
CONCLUSION: Baicalin alleviates Ang II-associated vascular remodelling, at least in part, by reprogramming gut microbial ecology, increasing luminal butyrate availability, promoting regulatory immune responses, and suppressing VSMC proliferative signalling.
METHODS: We utilized an Angiotensin II-induced hypertensive mouse model, employing broad-spectrum antibiotics, 16S rRNA sequencing, metabolomics, and in vitro co-culture assays to map the gut-immune-vascular axis.
RESULTS: Oral Baicalin significantly attenuated Ang II-induced blood pressure elevation and improved the intestinal barrier integrity. Antibiotic-induced microbiota depletion substantially weakened these protective effects, supporting a major microbiota contribution under the present experimental conditions. Baicalin reshaped the gut microbial community, enriched SCFA-supporting taxa, and restored a putative butyrate-associated microbial signature, enriching Akkermansia and Lactobacillus accompanied by increased cecal butyrate levels. Exogenous sodium butyrate recapitulated several major protective features of Baicalin treatment, including expansion of Foxp3+ regulatory T cells in mesenteric lymph nodes. These immune changes were accompanied by increased Foxp3+ regulatory immune-cell accumulation in the aortic adventitia. In vitro, butyrate-licensed Tregs suppressed Ang II-induced vascular smooth muscle cell (VSMC) proliferative responses, at least partly through IL-10-mediated inhibition of MAPK/ERK signalling.
CONCLUSION: Baicalin alleviates Ang II-associated vascular remodelling, at least in part, by reprogramming gut microbial ecology, increasing luminal butyrate availability, promoting regulatory immune responses, and suppressing VSMC proliferative signalling.