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Войти в исследования Pakistan journal of pharmaceutical sciences · 2026
Platycodin D alleviates myocardial ischemia-reperfusion injury by suppressing aberrant mitophagy.
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Li Jiang, Xu Chengyang
Аннотация
BACKGROUND: Myocardial ischemia-reperfusion (I/R) injury represents a critical complication in cardiovascular diseases, profoundly influencing patient prognosis.
OBJECTIVES: This study endeavors to elucidate the protective mechanisms and effects of Platycodin-D (PD) on myocardial ischemia-reperfusion injury (MIRI).
METHODS: A rat model of myocardial ischemia-reperfusion was employed to assess the impact of PD treatment on cardiac performance, myocardial injury biomarkers (CK-MB, LDH, cTnI), and infarct size. Further mechanistic insights were gained through Western blot and JC-1 staining, which analyzed the modulation of the HIF-1α/BNIP3 signaling pathway and mitochondrial autophagy by PD.
RESULTS: PD treatment markedly improved cardiac function, decreased levels of myocardial injury biomarkers (CK-MB, LDH, cTnI), and reduced infarct size. Mechanistically, PD was found to regulate the HIF-1α/BNIP3 signaling pathway, inhibit mitochondrial autophagy, and enhance mitochondrial function. Western blot and JC-1 staining confirmed that PD increases mitochondrial membrane potential and reduces the number of damaged mitochondria in cardiomyocytes.
CONCLUSIONS: This study underscores the significant protective effects of Platycodin-D against myocardial ischemia-reperfusion injury, presenting a promising therapeutic approach for cardiovascular disease management.
OBJECTIVES: This study endeavors to elucidate the protective mechanisms and effects of Platycodin-D (PD) on myocardial ischemia-reperfusion injury (MIRI).
METHODS: A rat model of myocardial ischemia-reperfusion was employed to assess the impact of PD treatment on cardiac performance, myocardial injury biomarkers (CK-MB, LDH, cTnI), and infarct size. Further mechanistic insights were gained through Western blot and JC-1 staining, which analyzed the modulation of the HIF-1α/BNIP3 signaling pathway and mitochondrial autophagy by PD.
RESULTS: PD treatment markedly improved cardiac function, decreased levels of myocardial injury biomarkers (CK-MB, LDH, cTnI), and reduced infarct size. Mechanistically, PD was found to regulate the HIF-1α/BNIP3 signaling pathway, inhibit mitochondrial autophagy, and enhance mitochondrial function. Western blot and JC-1 staining confirmed that PD increases mitochondrial membrane potential and reduces the number of damaged mitochondria in cardiomyocytes.
CONCLUSIONS: This study underscores the significant protective effects of Platycodin-D against myocardial ischemia-reperfusion injury, presenting a promising therapeutic approach for cardiovascular disease management.
Предметные рубрики MeSH
AnimalsSaponinsMyocardial Reperfusion InjuryTriterpenesMaleSignal TransductionMitophagyHypoxia-Inducible Factor 1, alpha SubunitRatsRats, Sprague-DawleyMyocytes, CardiacMembrane ProteinsMembrane Potential, MitochondrialMitochondrial ProteinsDisease Models, AnimalMitochondria, HeartMyocardial Infarction