Salidroside protects against myocardial infarction via activating MIF-mediated mitochondrial quality control

Salidroside is a potential therapeutic agent for myocardial infarction (MI), exerting therapeutic effects on macrophage migration inhibitory factor (MIF)-regulated mitochondrial quality control. Our aim was to explore the mechanism through which the MIF pathway regulates salidroside-mediated resista...

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Published inChinese medicine Vol. 20; no. 1; pp. 27 - 15
Main Authors You, Baiyang, Zhang, Jie, Yang, Chuyan, Dun, Yaoshan, Qi, Dake, Long, Yuqiong, Cheng, Jing, Lin, Yuan, Zhou, Nanjiang, Zeng, Tanghao, Dong, Jie, Liu, Suixin
Format Journal Article
LanguageEnglish
Published England BioMed Central Ltd 28.02.2025
BioMed Central
BMC
Subjects
Animal models
Apoptosis
Cardiomyocyte apoptosis
Cardiomyocytes
Care and treatment
Coronary artery
Coronary vessels
Crystal structure
Cytokines
Development and progression
Echocardiography
Health aspects
Heart attack
Heart attacks
Heart failure
Hypoxia
Intubation
Ischemia
Kinases
Laboratory animals
Leukocyte migration
Ligands
Macrophage migration inhibitory factor
Medical prognosis
Mitochondria
Mitochondrial quality control
Mortality
Myocardial infarction
Myocardium
Ostomy
Physiological aspects
Proteins
Quality control
Salidroside
siRNA
Surgery
Transfection
Transmission electron microscopy
Veins & arteries
Ventilation
China
United States > US
Macrophage migration inhibitory factor
Myocardial infarction
Salidroside
Cardiomyocyte apoptosis
Mitochondrial quality control
Online AccessGet full text
ISSN1749-8546
1749-8546
DOI10.1186/s13020-025-01076-3

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Abstract Salidroside is a potential therapeutic agent for myocardial infarction (MI), exerting therapeutic effects on macrophage migration inhibitory factor (MIF)-regulated mitochondrial quality control. Our aim was to explore the mechanism through which the MIF pathway regulates salidroside-mediated resistance to hypoxia-induced cardiomyocyte apoptosis. Ligation surgery of the left anterior descending branch of the coronary artery was employed to establish a myocardial infarction mouse model. Salidroside at low and high doses was administered to the mice for 4 weeks after the surgery. Cardiac function was evaluated via echocardiography. Morphological changes, apoptosis, and mitochondrial damage in the myocardium were examined. For the cell experiments, cardiomyocytes were treated with salidroside under oxygen‒glucose deprivation (OGD) conditions and were either treated with recombinant MIF (rMIF) or transfected with Mif-siRNA. Subsequently, mitochondrial quality control and apoptosis were assessed. Salidroside enhanced mitochondrial quality control in MI model mice, mitigated apoptosis and improved cardiac dysfunction. Transmission electron microscopy indicated that there were fewer damaged mitochondria in the salidroside-treated mice compared with the control mice. MIF and downstream mitochondrial quality control pathways were activated in the mice treated with salidroside. Consistently, the cell experiments demonstrated that salidroside and rMIF alleviated apoptosis, improved impaired mitochondrial quality control in OGD-induced cells and activated MIF signaling in OGD-induced cells. However, these effects of salidroside were partially blocked by Mif-siRNA transfection. Salidroside alleviated myocardial apoptosis and ameliorated cardiac dysfunction in MI model mice through the MIF pathway and downstream mitochondrial quality control.
AbstractList Salidroside is a potential therapeutic agent for myocardial infarction (MI), exerting therapeutic effects on macrophage migration inhibitory factor (MIF)-regulated mitochondrial quality control. Our aim was to explore the mechanism through which the MIF pathway regulates salidroside-mediated resistance to hypoxia-induced cardiomyocyte apoptosis.BACKGROUNDSalidroside is a potential therapeutic agent for myocardial infarction (MI), exerting therapeutic effects on macrophage migration inhibitory factor (MIF)-regulated mitochondrial quality control. Our aim was to explore the mechanism through which the MIF pathway regulates salidroside-mediated resistance to hypoxia-induced cardiomyocyte apoptosis.Ligation surgery of the left anterior descending branch of the coronary artery was employed to establish a myocardial infarction mouse model. Salidroside at low and high doses was administered to the mice for 4 weeks after the surgery. Cardiac function was evaluated via echocardiography. Morphological changes, apoptosis, and mitochondrial damage in the myocardium were examined. For the cell experiments, cardiomyocytes were treated with salidroside under oxygen‒glucose deprivation (OGD) conditions and were either treated with recombinant MIF (rMIF) or transfected with Mif-siRNA. Subsequently, mitochondrial quality control and apoptosis were assessed.METHODSLigation surgery of the left anterior descending branch of the coronary artery was employed to establish a myocardial infarction mouse model. Salidroside at low and high doses was administered to the mice for 4 weeks after the surgery. Cardiac function was evaluated via echocardiography. Morphological changes, apoptosis, and mitochondrial damage in the myocardium were examined. For the cell experiments, cardiomyocytes were treated with salidroside under oxygen‒glucose deprivation (OGD) conditions and were either treated with recombinant MIF (rMIF) or transfected with Mif-siRNA. Subsequently, mitochondrial quality control and apoptosis were assessed.Salidroside enhanced mitochondrial quality control in MI model mice, mitigated apoptosis and improved cardiac dysfunction. Transmission electron microscopy indicated that there were fewer damaged mitochondria in the salidroside-treated mice compared with the control mice. MIF and downstream mitochondrial quality control pathways were activated in the mice treated with salidroside. Consistently, the cell experiments demonstrated that salidroside and rMIF alleviated apoptosis, improved impaired mitochondrial quality control in OGD-induced cells and activated MIF signaling in OGD-induced cells. However, these effects of salidroside were partially blocked by Mif-siRNA transfection.RESULTSSalidroside enhanced mitochondrial quality control in MI model mice, mitigated apoptosis and improved cardiac dysfunction. Transmission electron microscopy indicated that there were fewer damaged mitochondria in the salidroside-treated mice compared with the control mice. MIF and downstream mitochondrial quality control pathways were activated in the mice treated with salidroside. Consistently, the cell experiments demonstrated that salidroside and rMIF alleviated apoptosis, improved impaired mitochondrial quality control in OGD-induced cells and activated MIF signaling in OGD-induced cells. However, these effects of salidroside were partially blocked by Mif-siRNA transfection.Salidroside alleviated myocardial apoptosis and ameliorated cardiac dysfunction in MI model mice through the MIF pathway and downstream mitochondrial quality control.CONCLUSIONSalidroside alleviated myocardial apoptosis and ameliorated cardiac dysfunction in MI model mice through the MIF pathway and downstream mitochondrial quality control.
BackgroundSalidroside is a potential therapeutic agent for myocardial infarction (MI), exerting therapeutic effects on macrophage migration inhibitory factor (MIF)-regulated mitochondrial quality control. Our aim was to explore the mechanism through which the MIF pathway regulates salidroside-mediated resistance to hypoxia-induced cardiomyocyte apoptosis.MethodsLigation surgery of the left anterior descending branch of the coronary artery was employed to establish a myocardial infarction mouse model. Salidroside at low and high doses was administered to the mice for 4 weeks after the surgery. Cardiac function was evaluated via echocardiography. Morphological changes, apoptosis, and mitochondrial damage in the myocardium were examined. For the cell experiments, cardiomyocytes were treated with salidroside under oxygen‒glucose deprivation (OGD) conditions and were either treated with recombinant MIF (rMIF) or transfected with Mif-siRNA. Subsequently, mitochondrial quality control and apoptosis were assessed.ResultsSalidroside enhanced mitochondrial quality control in MI model mice, mitigated apoptosis and improved cardiac dysfunction. Transmission electron microscopy indicated that there were fewer damaged mitochondria in the salidroside-treated mice compared with the control mice. MIF and downstream mitochondrial quality control pathways were activated in the mice treated with salidroside. Consistently, the cell experiments demonstrated that salidroside and rMIF alleviated apoptosis, improved impaired mitochondrial quality control in OGD-induced cells and activated MIF signaling in OGD-induced cells. However, these effects of salidroside were partially blocked by Mif-siRNA transfection.ConclusionSalidroside alleviated myocardial apoptosis and ameliorated cardiac dysfunction in MI model mice through the MIF pathway and downstream mitochondrial quality control.
Background Salidroside is a potential therapeutic agent for myocardial infarction (MI), exerting therapeutic effects on macrophage migration inhibitory factor (MIF)-regulated mitochondrial quality control. Our aim was to explore the mechanism through which the MIF pathway regulates salidroside-mediated resistance to hypoxia-induced cardiomyocyte apoptosis. Methods Ligation surgery of the left anterior descending branch of the coronary artery was employed to establish a myocardial infarction mouse model. Salidroside at low and high doses was administered to the mice for 4 weeks after the surgery. Cardiac function was evaluated via echocardiography. Morphological changes, apoptosis, and mitochondrial damage in the myocardium were examined. For the cell experiments, cardiomyocytes were treated with salidroside under oxygen-glucose deprivation (OGD) conditions and were either treated with recombinant MIF (rMIF) or transfected with Mif-siRNA. Subsequently, mitochondrial quality control and apoptosis were assessed. Results Salidroside enhanced mitochondrial quality control in MI model mice, mitigated apoptosis and improved cardiac dysfunction. Transmission electron microscopy indicated that there were fewer damaged mitochondria in the salidroside-treated mice compared with the control mice. MIF and downstream mitochondrial quality control pathways were activated in the mice treated with salidroside. Consistently, the cell experiments demonstrated that salidroside and rMIF alleviated apoptosis, improved impaired mitochondrial quality control in OGD-induced cells and activated MIF signaling in OGD-induced cells. However, these effects of salidroside were partially blocked by Mif-siRNA transfection. Conclusion Salidroside alleviated myocardial apoptosis and ameliorated cardiac dysfunction in MI model mice through the MIF pathway and downstream mitochondrial quality control. Keywords: Salidroside, Macrophage migration inhibitory factor, Myocardial infarction, Cardiomyocyte apoptosis, Mitochondrial quality control
Abstract Background Salidroside is a potential therapeutic agent for myocardial infarction (MI), exerting therapeutic effects on macrophage migration inhibitory factor (MIF)-regulated mitochondrial quality control. Our aim was to explore the mechanism through which the MIF pathway regulates salidroside-mediated resistance to hypoxia-induced cardiomyocyte apoptosis. Methods Ligation surgery of the left anterior descending branch of the coronary artery was employed to establish a myocardial infarction mouse model. Salidroside at low and high doses was administered to the mice for 4 weeks after the surgery. Cardiac function was evaluated via echocardiography. Morphological changes, apoptosis, and mitochondrial damage in the myocardium were examined. For the cell experiments, cardiomyocytes were treated with salidroside under oxygen‒glucose deprivation (OGD) conditions and were either treated with recombinant MIF (rMIF) or transfected with Mif-siRNA. Subsequently, mitochondrial quality control and apoptosis were assessed. Results Salidroside enhanced mitochondrial quality control in MI model mice, mitigated apoptosis and improved cardiac dysfunction. Transmission electron microscopy indicated that there were fewer damaged mitochondria in the salidroside-treated mice compared with the control mice. MIF and downstream mitochondrial quality control pathways were activated in the mice treated with salidroside. Consistently, the cell experiments demonstrated that salidroside and rMIF alleviated apoptosis, improved impaired mitochondrial quality control in OGD-induced cells and activated MIF signaling in OGD-induced cells. However, these effects of salidroside were partially blocked by Mif-siRNA transfection. Conclusion Salidroside alleviated myocardial apoptosis and ameliorated cardiac dysfunction in MI model mice through the MIF pathway and downstream mitochondrial quality control.
Salidroside is a potential therapeutic agent for myocardial infarction (MI), exerting therapeutic effects on macrophage migration inhibitory factor (MIF)-regulated mitochondrial quality control. Our aim was to explore the mechanism through which the MIF pathway regulates salidroside-mediated resistance to hypoxia-induced cardiomyocyte apoptosis. Ligation surgery of the left anterior descending branch of the coronary artery was employed to establish a myocardial infarction mouse model. Salidroside at low and high doses was administered to the mice for 4 weeks after the surgery. Cardiac function was evaluated via echocardiography. Morphological changes, apoptosis, and mitochondrial damage in the myocardium were examined. For the cell experiments, cardiomyocytes were treated with salidroside under oxygen-glucose deprivation (OGD) conditions and were either treated with recombinant MIF (rMIF) or transfected with Mif-siRNA. Subsequently, mitochondrial quality control and apoptosis were assessed. Salidroside enhanced mitochondrial quality control in MI model mice, mitigated apoptosis and improved cardiac dysfunction. Transmission electron microscopy indicated that there were fewer damaged mitochondria in the salidroside-treated mice compared with the control mice. MIF and downstream mitochondrial quality control pathways were activated in the mice treated with salidroside. Consistently, the cell experiments demonstrated that salidroside and rMIF alleviated apoptosis, improved impaired mitochondrial quality control in OGD-induced cells and activated MIF signaling in OGD-induced cells. However, these effects of salidroside were partially blocked by Mif-siRNA transfection. Salidroside alleviated myocardial apoptosis and ameliorated cardiac dysfunction in MI model mice through the MIF pathway and downstream mitochondrial quality control.
Salidroside is a potential therapeutic agent for myocardial infarction (MI), exerting therapeutic effects on macrophage migration inhibitory factor (MIF)-regulated mitochondrial quality control. Our aim was to explore the mechanism through which the MIF pathway regulates salidroside-mediated resistance to hypoxia-induced cardiomyocyte apoptosis. Ligation surgery of the left anterior descending branch of the coronary artery was employed to establish a myocardial infarction mouse model. Salidroside at low and high doses was administered to the mice for 4 weeks after the surgery. Cardiac function was evaluated via echocardiography. Morphological changes, apoptosis, and mitochondrial damage in the myocardium were examined. For the cell experiments, cardiomyocytes were treated with salidroside under oxygen‒glucose deprivation (OGD) conditions and were either treated with recombinant MIF (rMIF) or transfected with Mif-siRNA. Subsequently, mitochondrial quality control and apoptosis were assessed. Salidroside enhanced mitochondrial quality control in MI model mice, mitigated apoptosis and improved cardiac dysfunction. Transmission electron microscopy indicated that there were fewer damaged mitochondria in the salidroside-treated mice compared with the control mice. MIF and downstream mitochondrial quality control pathways were activated in the mice treated with salidroside. Consistently, the cell experiments demonstrated that salidroside and rMIF alleviated apoptosis, improved impaired mitochondrial quality control in OGD-induced cells and activated MIF signaling in OGD-induced cells. However, these effects of salidroside were partially blocked by Mif-siRNA transfection. Salidroside alleviated myocardial apoptosis and ameliorated cardiac dysfunction in MI model mice through the MIF pathway and downstream mitochondrial quality control.
ArticleNumber 27
Audience Academic
Author Lin, Yuan
Dong, Jie
Qi, Dake
Long, Yuqiong
Dun, Yaoshan
Zeng, Tanghao
Liu, Suixin
Zhou, Nanjiang
Yang, Chuyan
Cheng, Jing
Zhang, Jie
You, Baiyang
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Keywords Macrophage migration inhibitory factor
Myocardial infarction
Salidroside
Cardiomyocyte apoptosis
Mitochondrial quality control
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Snippet Salidroside is a potential therapeutic agent for myocardial infarction (MI), exerting therapeutic effects on macrophage migration inhibitory factor...
Background Salidroside is a potential therapeutic agent for myocardial infarction (MI), exerting therapeutic effects on macrophage migration inhibitory factor...
BackgroundSalidroside is a potential therapeutic agent for myocardial infarction (MI), exerting therapeutic effects on macrophage migration inhibitory factor...
Abstract Background Salidroside is a potential therapeutic agent for myocardial infarction (MI), exerting therapeutic effects on macrophage migration...
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SubjectTerms Animal models
Apoptosis
Cardiomyocyte apoptosis
Cardiomyocytes
Care and treatment
Coronary artery
Coronary vessels
Crystal structure
Cytokines
Development and progression
Echocardiography
Health aspects
Heart attack
Heart attacks
Heart failure
Hypoxia
Intubation
Ischemia
Kinases
Laboratory animals
Leukocyte migration
Ligands
Macrophage migration inhibitory factor
Medical prognosis
Mitochondria
Mitochondrial quality control
Mortality
Myocardial infarction
Myocardium
Ostomy
Physiological aspects
Proteins
Quality control
Salidroside
siRNA
Surgery
Transfection
Transmission electron microscopy
Veins & arteries
Ventilation
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Title Salidroside protects against myocardial infarction via activating MIF-mediated mitochondrial quality control
URI https://www.ncbi.nlm.nih.gov/pubmed/40016840
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