Danqi Tablet (丹七片) Regulates Energy Metabolism in Ischemic Heart Rat Model through AMPK/SIRT1-PGC-1α Pathway

Meng, Hui; Wang, Qiyan; Li, Ning; He, Hao; Lü, Wei; Wang, Qi-xin; Sun, Xiaoqian; Jiao, Shihong; Wang, Yong; Tu, Pengfei

doi:10.1007/s11655-019-3040-8

Cited by 11 publications

(9 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…An existing study has revealed that TMZ decreases the myocardial infarct size and shifts metabolism through regulation of the AMPK and ERK signaling pathways ( Liu et al, 2016 ). The AMPK/SIRT1/PGC-1α pathway is involved in the regulation of energy metabolism in an ischemic heart rat model ( Meng et al, 2019 ). Existing results have suggested that SIRT1 inhibits apoptosis from hypoxic stress and diabetic cardiomyopathy ( Guo et al, 2015 ; Luo et al, 2019 ).…”

Section: Discussionmentioning

confidence: 99%

Function and Mechanism of Trimetazidine in Myocardial Infarction-Induced Myocardial Energy Metabolism Disorder Through the SIRT1–AMPK Pathway

et al. 2021

View full text Add to dashboard Cite

Myocardial energy metabolism (MEM) is an important factor of myocardial injury. Trimetazidine (TMZ) provides protection against myocardial ischemia/reperfusion injury. The current study set out to evaluate the effect and mechanism of TMZ on MEM disorder induced by myocardial infarction (MI). Firstly, a MI mouse model was established by coronary artery ligation, which was then treated with different concentrations of TMZ (5, 10, and 20 mg kg–1 day–1). The results suggested that TMZ reduced the heart/weight ratio in a concentration-dependent manner. TMZ also reduced the levels of Bax and cleaved caspase-3 and promoted Bcl-2 expression. In addition, TMZ augmented adenosine triphosphate (ATP) production and superoxide dismutase (SOD) activity induced by MI and decreased the levels of lipid peroxide (LPO), free fatty acids (FFA), and nitric oxide (NO) in a concentration-dependent manner (all P < 0.05). Furthermore, an H2O2-induced cell injury model was established and treated with different concentrations of TMZ (1, 5, and 10 μM). The results showed that SIRT1 overexpression promoted ATP production and reactive oxygen species (ROS) activity and reduced the levels of LPO, FFA, and NO in H9C2 cardiomyocytes treated with H2O2 and TMZ. Silencing SIRT1 suppressed ATP production and ROS activity and increased the levels of LPO, FFA, and NO (all P < 0.05). TMZ activated the SIRT1–AMPK pathway by increasing SIRT1 expression and AMPK phosphorylation. In conclusion, TMZ inhibited MI-induced myocardial apoptosis and MEM disorder by activating the SIRT1–AMPK pathway.

show abstract

Section: Discussionmentioning

confidence: 99%

Function and Mechanism of Trimetazidine in Myocardial Infarction-Induced Myocardial Energy Metabolism Disorder Through the SIRT1–AMPK Pathway

et al. 2021

View full text Add to dashboard Cite

show abstract

“…They found that the increase of ATP content and PPARγ expression of DQP could be inhibited by T0070907 in OGD/R-induced H9c2 cell injury. Besides, DQP has also been suggested to regulate energy metabolism in rat ischemic myocardium through the AMPK/SIRT1-PGC-1α signaling pathway ( Meng et al., 2019 ).…”

Section: Modulatory Effects Of Chinese Herbal Medicines On Energy Metmentioning

confidence: 99%

Modulatory Effects of Chinese Herbal Medicines on Energy Metabolism in Ischemic Heart Diseases

et al. 2020

Front. Pharmacol.

View full text Add to dashboard Cite

Ischemic heart disease (IHD), a major global public health problem, is associated with high morbidity and mortality. Although the very best of modern approaches have proven effective in reducing morbidity and mortality, the poor prognosis of patients with IHD remains a major clinical concern. Cardiac energy metabolism is increasingly recognized as having a role in the pathogenesis of IHD, inducing metabolic substrate alterations, mitochondrial dysfunction, impaired function of the mitochondrial electron transport chain, and deprivation of cardiac energy. Factors involved in cardiac energy metabolism provide potential therapeutic targets for the treatment of IHD. Chinese herbal medicines (CHMs) have a long history of use in the prevention and treatment of cardiovascular diseases with multi-component, multi-target, and multi-signaling. Increasing evidence suggests that Chinese herbal medicines may improve myocardial ischemia through modulating cardiac energy metabolism. Here, we describe the possible targets and pathways of cardiac energy metabolism for CHMs, and appraise the modulatory effects of CHMs on energy metabolism in IHD. Especially, this review focuses on summarizing the metabolic effects and the underlying mechanisms of Chinese herbal medicines (including herbs, major bioactive components, and formulas) in IHD. In addition, we also discuss the current limitations and the major challenges for research investigating the use of CHMs in the treatment of cardiovascular diseases.

show abstract

“…In addition, AMPK/ Sirt1/PGC-1α seems to be also correlated with the progression of DM (Jiang et al 2015;Hou et al 2017;Huang et al 2019;Liao et al 2019;Yap et al 2020). More importantly, numerous studies have demonstrated that the activation of the AMPK/Sirt1/PGC-1α pathway attenuates MI/RI in a rat model (Meng et al 2019;Tian et al 2019). Interestingly, some pharmacological agents such as metformin and catalpol can enhance insulin sensitivity via activation of the AMPK/Sirt1/PGC-1α pathway (Banerjee et al 2016;Yap et al 2020).…”

Section: Introductionmentioning

confidence: 99%

Aerobic exercise ameliorates myocardial ischemia/reperfusion injury and thrombosis of diabetic rats via activation of AMPK/Sirt1/PGC-1α pathway

Wang¹

2022

gpb

View full text Add to dashboard Cite

This current work is aimed to make investigations for the action mechanism of aerobic exercise in rats with type 2 diabetes mellitus (T2DM) after myocardial ischemia/reperfusion injury (MI/RI). The high-fat diet was used to induce T2DM in male Wistar rats. After treatments, the rats in the exercise groups were underwent swimming training for 8 weeks. Two days later, all the rats were subjected to perform MI/RI experiments via left anterior descending artery ligation and reperfusion. The blood samples and myocardial tissues were collected for biochemistry analysis and histology assessment. The results demonstrated that aerobic exercise reduced the levels of serum glucose, total cholesterol (TC), triglyceride (TG), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), and thrombosis in T2DM rats. In addition, aerobic exercise further decreased the levels of myocardial injury markers and also repressed inflammation responses. Furthermore, the AMP-activated protein kinase (AMPK)/silent information regulator factor 2-related enzyme 1 (Sirt1)/peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) pathway could be activated by aerobic exercise. In a word, aerobic exercise may attenuate myocardial ischemia/reperfusion injury and repress thrombosis via activation of the AMPK/Sirt1/ PGC-1α pathway in DM rats.

show abstract

Danqi Tablet (丹七片) Regulates Energy Metabolism in Ischemic Heart Rat Model through AMPK/SIRT1-PGC-1α Pathway

Cited by 11 publications

References 25 publications

Function and Mechanism of Trimetazidine in Myocardial Infarction-Induced Myocardial Energy Metabolism Disorder Through the SIRT1–AMPK Pathway

Function and Mechanism of Trimetazidine in Myocardial Infarction-Induced Myocardial Energy Metabolism Disorder Through the SIRT1–AMPK Pathway

Modulatory Effects of Chinese Herbal Medicines on Energy Metabolism in Ischemic Heart Diseases

Aerobic exercise ameliorates myocardial ischemia/reperfusion injury and thrombosis of diabetic rats via activation of AMPK/Sirt1/PGC-1α pathway

Contact Info

Product

Resources

About