Phytomedicine : international journal of phytotherapy and phytopharmacology · 2026
Hongqi Shenmai Yin attenuates adverse cardiac remodeling following myocardial infarction via inhibition of STING-dependent PANoptosis.
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.
Zhang Meng, Chen Zhaoyang, Yin Xuehui, Bo Haohao, Mao Chenhan, Gong Juexiao, Zhang Xinyue, Gao Xin, Wang Xindong
Аннотация
BACKGROUND: Pathological ventricular remodeling following myocardial infarction (MI) severely impacts long term prognosis of patients, yet effective interventions to halt its progression remain limited. Hongqi Shenmai Yin (HSY) has been used in clinical practice for many years, can improve cardiac function in MI patients. However, its underlying therapeutic mechanisms remain unclear.
PURPOSE: This study aimed to determine whether HSY alleviates adverse cardiac remodeling following MI by inhibiting stimulator of interferon genes (STING)-dependent PANoptosis.
METHODS: The MI model was established by ligating the left anterior descending coronary artery (LAD) in rats. Ultra performance liquid chromatography-tandem mass spectrometry (UPLC-MS) identified bioactive compounds in HSY. Cardiac function, hypertrophy, and fibrosis were assessed via echocardiography and histological staining. ELISA measured cardiac injury biomarkers, inflammatory cytokines, and oxidative stress markers. Transcriptomic analyses identified potential HSY targets in post-MI remodeling. Molecular docking and surface plasmon resonance (SPR) assessed binding interactions between HSY's key active components and STING. Mechanistic rescue experiments determined whether HSY regulates PANoptosis via STING inhibition. Functional studies were further conducted by transfecting H9c2 cardiomyocytes with lentivirus vectors encoding STING-overexpression.
RESULTS: HSY attenuated inflammation, oxidative stress, and adverse remodeling while improving cardiac function post-MI. UPLC-MS identified 107 major HSY constituents. Transcriptomics linked HSY's cardioprotective effects to STING signaling and PANoptosis modulation. Molecular docking and SPR confirmed strong binding affinity between HSY's primary active compounds and STING. Both in vivo and in vitro experiments revealed that HSY suppressed STING-induced ZBP1-PANoptosome assembly, downregulating PANoptosis-associated proteins (p-MLKL, p-RIPK1, p-RIPK3, GSDMD-NT, GSDME-NT, Cle-CASP1, Cle-CASP3, Cle-CASP8) in post-MI remodeling.
CONCLUSION: HSY attenuated adverse cardiac remodeling following MI by inhibiting STING-mediated ZBP1-PANoptosome assembly and subsequent PANoptosis. These findings supported HSY's clinical potential in treating post-MI cardiac remodeling.
PURPOSE: This study aimed to determine whether HSY alleviates adverse cardiac remodeling following MI by inhibiting stimulator of interferon genes (STING)-dependent PANoptosis.
METHODS: The MI model was established by ligating the left anterior descending coronary artery (LAD) in rats. Ultra performance liquid chromatography-tandem mass spectrometry (UPLC-MS) identified bioactive compounds in HSY. Cardiac function, hypertrophy, and fibrosis were assessed via echocardiography and histological staining. ELISA measured cardiac injury biomarkers, inflammatory cytokines, and oxidative stress markers. Transcriptomic analyses identified potential HSY targets in post-MI remodeling. Molecular docking and surface plasmon resonance (SPR) assessed binding interactions between HSY's key active components and STING. Mechanistic rescue experiments determined whether HSY regulates PANoptosis via STING inhibition. Functional studies were further conducted by transfecting H9c2 cardiomyocytes with lentivirus vectors encoding STING-overexpression.
RESULTS: HSY attenuated inflammation, oxidative stress, and adverse remodeling while improving cardiac function post-MI. UPLC-MS identified 107 major HSY constituents. Transcriptomics linked HSY's cardioprotective effects to STING signaling and PANoptosis modulation. Molecular docking and SPR confirmed strong binding affinity between HSY's primary active compounds and STING. Both in vivo and in vitro experiments revealed that HSY suppressed STING-induced ZBP1-PANoptosome assembly, downregulating PANoptosis-associated proteins (p-MLKL, p-RIPK1, p-RIPK3, GSDMD-NT, GSDME-NT, Cle-CASP1, Cle-CASP3, Cle-CASP8) in post-MI remodeling.
CONCLUSION: HSY attenuated adverse cardiac remodeling following MI by inhibiting STING-mediated ZBP1-PANoptosome assembly and subsequent PANoptosis. These findings supported HSY's clinical potential in treating post-MI cardiac remodeling.