Phytomedicine : international journal of phytotherapy and phytopharmacology · 2026
Dangshen formula Shengmai-Yin suppresses atherosclerosis through restoring the gut microbiota and homeostatic efferocytosis.
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Li Yang, Wang Feixia, Hu Mengru, Li Yu, Xia Siwei, Zhou Ya, Li Weitong, Chen Li, Yan Li, Sun Pingping, Wang Libin, Liu Gang, Wu Di, Lu Tao, Zhang Feng, Zheng Shizhong, Li Anning, Lu Tulin
Аннотация
BACKGROUND & AIMS: Atherosclerosis (AS) is a chronic progressive vascular disease characterized by lipid deposition and aortic inflammation. On the basis of traditional Chinese medicine (TCM) theory, the Dangshen Formula Shengmai-Yin (DS-SMY) has demonstrated unique advantages in treating AS. However, the mechanism by which DS-SMY affects AS has not been revealed.
METHODS: In this study, high-fat diet-induced apolipoprotein E knockout (ApoE-/-) mice were used to construct AS models. The effects of DS-SMY on aortic collagen deposition and inflammatory infiltration were investigated, and atorvastatin (Ato) was used as a positive control. The composition of the gut microbiota was assessed using high-throughput sequencing of the 16S rRNA gene. Colon morphology was observed via TEM, and apoptosis was assessed with TUNEL staining. The main component of DS-SMY in drug-containing serum was determined by HPLC. The effects of DS-SMY components (lobetyolin and schisandrin) were evaluated in PA-induced RAW 264.7 cells using WB, ELISA, and RT-qPCR.
RESULTS: Compared with Ato, DS-SMY also had a therapeutic effect on ApoE-/- mice. In addition, DS-SMY inhibited M1 polarization of macrophages in ApoE-/- mice. Additionally, the results demonstrated that DS-SMY alleviated intestinal inflammation and promoted the formation of colon tight junctions. Furthermore, changes in the gut microbiota composition in ApoE-/- mice after DS-SMY treatment were sufficient to induce changes in colon inflammation. Mechanistically, the results revealed that DS-SMY components suppressed proinflammatory cytokine expression and enhanced macrophage efferocytosis. Furthermore, supplementation with butyric acid (a gut microbiota-derived metabolite) enhanced the effect of DS-SMY, which demonstrated that the effect of DS-SMY involved microbiota-dependent mechanisms.
CONCLUSION: In summary, DS-SMY can alleviate atherogenic dyslipidemia and pathological inflammation in AS by targeting the gut microbiota and homeostatic efferocytosis and is accordingly a potential therapeutic agent for AS.
METHODS: In this study, high-fat diet-induced apolipoprotein E knockout (ApoE-/-) mice were used to construct AS models. The effects of DS-SMY on aortic collagen deposition and inflammatory infiltration were investigated, and atorvastatin (Ato) was used as a positive control. The composition of the gut microbiota was assessed using high-throughput sequencing of the 16S rRNA gene. Colon morphology was observed via TEM, and apoptosis was assessed with TUNEL staining. The main component of DS-SMY in drug-containing serum was determined by HPLC. The effects of DS-SMY components (lobetyolin and schisandrin) were evaluated in PA-induced RAW 264.7 cells using WB, ELISA, and RT-qPCR.
RESULTS: Compared with Ato, DS-SMY also had a therapeutic effect on ApoE-/- mice. In addition, DS-SMY inhibited M1 polarization of macrophages in ApoE-/- mice. Additionally, the results demonstrated that DS-SMY alleviated intestinal inflammation and promoted the formation of colon tight junctions. Furthermore, changes in the gut microbiota composition in ApoE-/- mice after DS-SMY treatment were sufficient to induce changes in colon inflammation. Mechanistically, the results revealed that DS-SMY components suppressed proinflammatory cytokine expression and enhanced macrophage efferocytosis. Furthermore, supplementation with butyric acid (a gut microbiota-derived metabolite) enhanced the effect of DS-SMY, which demonstrated that the effect of DS-SMY involved microbiota-dependent mechanisms.
CONCLUSION: In summary, DS-SMY can alleviate atherogenic dyslipidemia and pathological inflammation in AS by targeting the gut microbiota and homeostatic efferocytosis and is accordingly a potential therapeutic agent for AS.