Clinical and investigative medicine. Medecine clinique et experimentale · 2025
Crocin ameliorates hypertension-induced cardiac hypertrophy and apoptosis by activating AMPKα signalling.
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Luo Dan, Wang Jueyan, Zheng Shijiao, Li Wei, Yu Bo, Peng Huan, Gui Feng, Mao Bing, Chen Zhen
Аннотация
PURPOSE: Cardiac hypertrophy is a critical contributor to heart failure. Therapies that effectively manage cardiac hypertrophy are still inadequate. Crocin is a natural component of saffron, and its beneficial properties have been previously documented. This study aimed to investigate the role of crocin in cardiac hypertrophy and apoptosis and its related mechanisms.
METHODS: Sprague-Dawley rats were infused with angiotensin II (Ang II; 520 ng/kg/min) or normal saline and then intraperitoneally injected with crocin (40 mg/kg) or dimethyl sulfoxide for 4 weeks. Systolic and diastolic blood pressure were recorded. Cardiac hypertrophy was evaluated by echocardiography, heart weight, hematoxylin-eosin staining, TUNEL assay, and gene expression. For in vitro studies, H9C2 cells were treated with Ang II (1 μM) for 48 hours to induce cardiac hypertrophy-like conditions. An immunofluorescence assay was used for [Formula: see text]-actinin staining. reverse transcription quantitative real-time polymerase chain reaction was performed to measure the expression of hypertrophic markers, and western blotting was used to detect apoptosis and underlying mechanisms.
RESULTS: Our findings revealed that crocin attenuated diastolic dysfunction, cardiac hypertrophy, and apoptosis caused by Ang II in vivo. Additionally, crocin prevented Ang II-stimulated cardiomyocyte enlargement and apoptosis in vitro. Mechanistically, crocin induced AMP-activated protein kinase (AMPK)[Formula: see text] activation and mTOR/p70S6K inhibition in cellular and animal models of cardiac hypertrophy. Moreover, AMPK inhibition abolished the anti-hypertrophic effect of crocin in vitro, while mTOR inhibition enhanced the protective effect of crocin against Ang II-induced cardiomyocyte hypertrophy.
CONCLUSION: This study demonstrates that crocin can ameliorate Ang II-stimulated cardiac hypertrophy in vivo and in vitro by regulating AMPK[Formula: see text]/mTOR/ p70S6K signalling.
METHODS: Sprague-Dawley rats were infused with angiotensin II (Ang II; 520 ng/kg/min) or normal saline and then intraperitoneally injected with crocin (40 mg/kg) or dimethyl sulfoxide for 4 weeks. Systolic and diastolic blood pressure were recorded. Cardiac hypertrophy was evaluated by echocardiography, heart weight, hematoxylin-eosin staining, TUNEL assay, and gene expression. For in vitro studies, H9C2 cells were treated with Ang II (1 μM) for 48 hours to induce cardiac hypertrophy-like conditions. An immunofluorescence assay was used for [Formula: see text]-actinin staining. reverse transcription quantitative real-time polymerase chain reaction was performed to measure the expression of hypertrophic markers, and western blotting was used to detect apoptosis and underlying mechanisms.
RESULTS: Our findings revealed that crocin attenuated diastolic dysfunction, cardiac hypertrophy, and apoptosis caused by Ang II in vivo. Additionally, crocin prevented Ang II-stimulated cardiomyocyte enlargement and apoptosis in vitro. Mechanistically, crocin induced AMP-activated protein kinase (AMPK)[Formula: see text] activation and mTOR/p70S6K inhibition in cellular and animal models of cardiac hypertrophy. Moreover, AMPK inhibition abolished the anti-hypertrophic effect of crocin in vitro, while mTOR inhibition enhanced the protective effect of crocin against Ang II-induced cardiomyocyte hypertrophy.
CONCLUSION: This study demonstrates that crocin can ameliorate Ang II-stimulated cardiac hypertrophy in vivo and in vitro by regulating AMPK[Formula: see text]/mTOR/ p70S6K signalling.