Phytomedicine : international journal of phytotherapy and phytopharmacology · 2026
Ningxintong and its active component calycosin stabilize vulnerable atherosclerotic plaques by targeting SIRT7 and inhibiting pyroptosis.
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Li Rui, Huang Xia, Wang Bingqian, Cao Xuran, Chen Zhiliang, Zhang Li, Gu Ning
Аннотация
OBJECTIVE: To investigate the regulatory effect of Ningxintong (NXT) on monocyte/macrophage pyroptosis in atherosclerosis (AS), elucidate its molecular mechanisms, and identify its key active components.
METHODS: The expression of inflammation- and pyroptosis-related molecules was detected in peripheral blood monocytes from patients with AS. An atherosclerotic vulnerable plaque (AS-VP) mouse model was established to evaluate the effects of NXT on blood lipid levels, plaque formation, and stability. miR-125b overexpression/knockdown, transcriptome sequencing, dual-luciferase reporter assays, SIRT7 inhibitor treatment, and in vivo/in vitro functional experiments were used to identify the active components in NXT and explore their potential pharmacological mechanisms using molecular dynamics simulations combined with in vivo and in vitro experiments.
RESULTS: The expression of inflammation- and pyroptosis-related molecules was significantly increased in the monocytes of patients with AS. NXT improved lipid metabolism disorders, reduced plaque volume, and inhibited the expression of NLRP3, gasdermin D (GSDMD), caspase-1, and interleukin (IL)-1β in monocytes from the mouse AS-VP model. The expression of miR-125b was significantly upregulated in AS, and its overexpression induced macrophage pyroptosis. Transcriptome sequencing and dual-luciferase experiments indicated that SIRT7 is a direct target gene of miR-125b. NXT inhibited macrophage pyroptosis, and its protective effect was significantly weakened after SIRT7 inhibition. Furthermore, calycosin (CA), an active component of NXT, upregulated SIRT7 expression, inhibited the p53- and NLRP3 inflammasome-related pyroptosis pathway, and improved plaque stability.
CONCLUSIONS: NXT and its active component CA may inhibit monocyte/macrophage pyroptosis by regulating the miR-125b/SIRT7/p53 signaling axis, thereby attenuating AS progression and stabilizing VPs, and may provide new experimental evidence and potential targets for the prevention and treatment of AS.
METHODS: The expression of inflammation- and pyroptosis-related molecules was detected in peripheral blood monocytes from patients with AS. An atherosclerotic vulnerable plaque (AS-VP) mouse model was established to evaluate the effects of NXT on blood lipid levels, plaque formation, and stability. miR-125b overexpression/knockdown, transcriptome sequencing, dual-luciferase reporter assays, SIRT7 inhibitor treatment, and in vivo/in vitro functional experiments were used to identify the active components in NXT and explore their potential pharmacological mechanisms using molecular dynamics simulations combined with in vivo and in vitro experiments.
RESULTS: The expression of inflammation- and pyroptosis-related molecules was significantly increased in the monocytes of patients with AS. NXT improved lipid metabolism disorders, reduced plaque volume, and inhibited the expression of NLRP3, gasdermin D (GSDMD), caspase-1, and interleukin (IL)-1β in monocytes from the mouse AS-VP model. The expression of miR-125b was significantly upregulated in AS, and its overexpression induced macrophage pyroptosis. Transcriptome sequencing and dual-luciferase experiments indicated that SIRT7 is a direct target gene of miR-125b. NXT inhibited macrophage pyroptosis, and its protective effect was significantly weakened after SIRT7 inhibition. Furthermore, calycosin (CA), an active component of NXT, upregulated SIRT7 expression, inhibited the p53- and NLRP3 inflammasome-related pyroptosis pathway, and improved plaque stability.
CONCLUSIONS: NXT and its active component CA may inhibit monocyte/macrophage pyroptosis by regulating the miR-125b/SIRT7/p53 signaling axis, thereby attenuating AS progression and stabilizing VPs, and may provide new experimental evidence and potential targets for the prevention and treatment of AS.