Frontiers in nutrition · 2026
Asiatic acid from Centella asiatica alleviates renal fibrosis: coordinated modulation of the gut-kidney axis and retinol metabolism.
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Zhu Liwei, Xu Ziyun, Chang Xiaoyan, Wu Jingyi, Chen Shutao, Jiang Yuanyuan, Guo Jiayu, Du Zhenfang, Chen Haiyong, Qiang Sheng
Аннотация
INTRODUCTION: Chronic kidney disease (CKD) is a progressive condition characterized by renal fibrosis, with limited therapeutic options. Asiatic acid (AA), a triterpenoid from Centella asiatica, has shown renoprotective potential, but its mechanisms remain unclear.
METHODS: An adenine-induced CKD mouse model was established in C57BL/6 mice. AA was administered orally at 10 or 30 mg/kg for 8 weeks. Antibiotic depletion experiments were performed to assess gut microbiota dependence. Renal function, histopathology, and fibrosis markers were evaluated. Multi-omics analyses integrated 16S rRNA sequencing, renal untargeted metabolomics, transcriptomics, and MetOrigin-based tracing. In vitro, human proximal tubular HK-2 cells were stimulated with TGF-β1 to assess the effects of key metabolites on fibrotic injury and oxidative stress.
RESULTS: AA significantly improved renal function, reduced tubular injury and collagen deposition, and restored gut barrier integrity. Antibiotic depletion experiments demonstrated that an intact gut microbiota is required for the renoprotective effects of AA supporting a functional link along the gut-kidney axis. AA remodeled the gut microbiota, notably enriching Lachnospiraceae NK4A136 group. Renal metabolomics and transcriptomics integration identified retinol metabolism as the key renal pathway rescued by AA, with 9-cis-retinal and 4-hydroxyretinoic acid negatively correlated with injury markers. In vitro, 9-cis-retinal suppressed TGF-β1-induced fibrotic markers and oxidative stress.
DISCUSSION: AA alleviates CKD in association with remodeling of the gut microbiota and reprogramming of renal retinol metabolism, supporting its potential as a dietary supplement for countering renal fibrosis and supporting kidney health.
METHODS: An adenine-induced CKD mouse model was established in C57BL/6 mice. AA was administered orally at 10 or 30 mg/kg for 8 weeks. Antibiotic depletion experiments were performed to assess gut microbiota dependence. Renal function, histopathology, and fibrosis markers were evaluated. Multi-omics analyses integrated 16S rRNA sequencing, renal untargeted metabolomics, transcriptomics, and MetOrigin-based tracing. In vitro, human proximal tubular HK-2 cells were stimulated with TGF-β1 to assess the effects of key metabolites on fibrotic injury and oxidative stress.
RESULTS: AA significantly improved renal function, reduced tubular injury and collagen deposition, and restored gut barrier integrity. Antibiotic depletion experiments demonstrated that an intact gut microbiota is required for the renoprotective effects of AA supporting a functional link along the gut-kidney axis. AA remodeled the gut microbiota, notably enriching Lachnospiraceae NK4A136 group. Renal metabolomics and transcriptomics integration identified retinol metabolism as the key renal pathway rescued by AA, with 9-cis-retinal and 4-hydroxyretinoic acid negatively correlated with injury markers. In vitro, 9-cis-retinal suppressed TGF-β1-induced fibrotic markers and oxidative stress.
DISCUSSION: AA alleviates CKD in association with remodeling of the gut microbiota and reprogramming of renal retinol metabolism, supporting its potential as a dietary supplement for countering renal fibrosis and supporting kidney health.