Cardioprotective effect of ginsenoside Rb1 via regulating metabolomics profiling and AMP-activated protein kinase-dependent mitophagy

Hu, Jingui; Zhang, Ling; Fu, Fei; Lai, Qiong; Zhang, Lu; Liu, Tao; Yu, Boyang; Kou, Junping; Li, Fang

doi:10.1016/j.jgr.2021.06.011

Cited by 18 publications

(7 citation statements)

References 45 publications

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“…Hu et al. found that GRb1 protects against acute myocardial ischemia injury by promoting mitophagy [32] . Consistently, in the present study, we found that GRg1 notably ameliorated morphological damage in the mitochondria and increased mitochondrial clearance within the mitophagosomes in comparison with the MI group, indicating the upregulation of mitophagy flux.…”

Section: Resultssupporting

confidence: 91%

Ginsenoside Rg1 Protects against Cardiac Remodeling in Heart Failure via SIRT1/PINK1/Parkin‐Mediated Mitophagy

Guan

Yin

Ding

et al. 2023

Chemistry & Biodiversity

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Adverse cardiac remodeling may lead to the development and progression of heart failure, which is lack of effective clinical treatment. Ginsenoside Rg1 (GRg1), a primary ingredient of Panax ginseng, protects against diverse cardiovascular disease, but its effects on cardiac remodeling remain unclear. Thus, we investigated the protective effect and mechanism of GRg1 on cardiac remodeling after myocardial infarction. GRg1 significantly ameliorated cardiac remodeling in mice with left anterior descending coronary artery ligation, reflected by reduced left ventricular dilation and decreased cardiac fibrosis, accompanied by improved cardiac function. Mechanistically, GRg1 considerably increased mitophagosomes formation, ameliorated cardiac mitochondria damage, and enhanced SIRT1/PINK1/Parkin-mediated mitophagy during cardiac remodeling. Consistently, GRg1 increased cell viability and attenuated apoptosis and fibrotic responses in H 2 O 2 -treated H9c2 cells by promoting the SIRT1/PINK1/Parkin axis. Furthermore, SIRT1-specific inhibitor (EX527) or the use of small interfering RNA against Parkin abolished the protective effect of GRg1 in vitro. These findings reveal a novel mechanism of GRg1 alleviating cardiac remodeling via enhancing SIRT1/PINK1/Parkin-mediated mitophagy.

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Section: Resultssupporting

confidence: 91%

Ginsenoside Rg1 Protects against Cardiac Remodeling in Heart Failure via SIRT1/PINK1/Parkin‐Mediated Mitophagy

Guan

Yin

Ding

et al. 2023

Chemistry & Biodiversity

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“…When mitochondrial health is compromised, in addition to mitochondrial dysfunction, mitochondrial morphology changes [37]. Mitochondrial morphology is regulated by mitophagy and mitochondrial dynamics [38]. Mitochondria exhibit a unique characteristic of constantly transitioning between elongated interconnected networks and fragmented disconnected arrangements.…”

Section: Discussionmentioning

confidence: 99%

Salidroside Alleviates Myocardial Ischemia Reperfusion by Balancing Mitochondrial Homeostasis via Nrf2

Yan,

Li,

Wang

et al. 2024

Journal of Food Biochemistry

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Salidroside (SAL), a phenylpropanoid glycoside compound mainly from Rhodiola rosea, showed potential effects on myocardial ischemia reperfusion (MIRI) in our previous studies. The primary objective of this investigation was to study the mechanism by which SAL preserves mitochondrial homeostasis in order to provide protection against MIRI. The impact of SAL on the hypoxia/reoxygenation (H/R)-induced H9c2 cells was detected by using CCK-8, LDH, and AST. The number, function, and morphology of mitochondria were examined by TEM, RT-qPCR, and western blot. The binding ability between SAL and Nrf2 was explored through molecular docking and the cell thermal shift assay. Combined with the Nrf2 inhibitor ML385, our results demonstrated that SAL promotes mitochondrial protection by activating Nrf2, decreasing oxidative stress, and altering the AMPK/PGC-1α/PPARα pathway. In addition, SAL elevates ATP levels and improves mitochondrial dynamics imbalance by inducing both autophagy and mitophagy. These findings highlight the potential therapeutic benefits of SAL for cardiac health and the mitigation of MIRI.

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“…KEGG pathway enrichment shows that AMPK pathway is down regulated in DOX + Rb group as compared with DOX group. Some studies reported that Dox trigger autophagy in mice heart by activating AMPK, while other reports showed AMPK has no change or even inhibition (19)(20)(21). Normally, phosphorylated AMPK activate ULK and deactivate the inhibition effect of mTOR to initiated the process of autophagy.…”

Section: Discussionmentioning

confidence: 99%

“…Studies have shown that Ginsenoside Rb1 protects acute ischemic myocardium through stimulation of AMPKa-mediated mitophagy and Ang II-induced abdominal aortic aneurysm via its anti-in ammatory effect [18]. Ginsenoside Rb1 exerts its antiin ammatory, anti-apoptosis, autophagy and energy regulation effect in acute ischemic myocardium, Ang II-induced abdominal aortic aneurysm and even diabetic cardiomyopathy [18][19][20]. Despite the numerous bene ts of Ginsenoside Rb1 on cardiovascular diseases, whether it can exert a protection role in DIC is unclear.…”

Section: Introductionmentioning

confidence: 99%

Ginsenoside Rb1 attenuates doxorubicin induced cardiotoxicity by suppressing autophagy and Nrf2 induced ferroptosis

Zhai,

Bai,

Peng

et al. 2024

Preprint

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Ginsenoside Rb1 (Rb1), an active component isolated from traditional Chinese medicine Ginseng, is beneficial to many cardiovascular diseases. However, whether it can protect against doxorubicin induced cardiotoxicity (DIC) is not clear yet. In this study, we aimed to investigate the role of Rb1 in DIC. Mice were injected with a single dose of doxorubicin (20mg/kg) to induce acute cardiotoxicity. Rb1 was given daily gavage to mice for 7 days. Changes in cardiac function, myocardium histopathology, oxidative stress, cardiomyocyte mitochondrion morphology as well as autophagy and ferroptosis pathway were studied to evaluate Rb1’s function on DIC. Meanwhile, RNA-seq analysis was performed to explore the potential underline molecular mechanism involved in Rb1’s function on DIC. We found that Rb1 treatment can improve survival rate and body weight in Dox treated mice group. Rb1 can attenuate Dox induced cardiac dysfunction and myocardium hypertrophy and interstitial fibrosis. The oxidative stress increase and cardiomyocyte mitochondrion destruction were improved by Rb1 treatment. Mechanism study found that Rb1’s beneficial role in DIC is through suppressing of autophagy and Nrf2 induced ferroptosis. This study shown that Ginsenoside Rb1 can protect against DIC by regulating autophagy and ferroptosis.

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Cardioprotective effect of ginsenoside Rb1 via regulating metabolomics profiling and AMP-activated protein kinase-dependent mitophagy

Cited by 18 publications

References 45 publications

Ginsenoside Rg1 Protects against Cardiac Remodeling in Heart Failure via SIRT1/PINK1/Parkin‐Mediated Mitophagy

Ginsenoside Rg1 Protects against Cardiac Remodeling in Heart Failure via SIRT1/PINK1/Parkin‐Mediated Mitophagy

Salidroside Alleviates Myocardial Ischemia Reperfusion by Balancing Mitochondrial Homeostasis via Nrf2

Ginsenoside Rb1 attenuates doxorubicin induced cardiotoxicity by suppressing autophagy and Nrf2 induced ferroptosis

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