Antiplatelet Therapy with Integrated Traditional Chinese and Western Medicine for Use in Myocardial Ischemia-Reperfusion Injury: A Review of Clinical Applications and Mechanisms

Li, Yuxuan; Li, Yan; Li, Bin; Liu, Yang; Zhang, Jingqian; Kuang, Wu; Lu, Jinjin; Cao, Zheng; Cui, Jie; Fan, Zongjing; Guo, Bin; Liu, Dong

doi:10.1155/2021/7409094

Cited by 5 publications

(5 citation statements)

References 51 publications

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“…Traditional Chinese medicine has been widely used in the treatment of myocardial ischaemia/reperfusion injury with safety and efficacy [12]. The bioactive flavonoids of Chinese medicine also exerted a cardioprotective effect against myocardial ischaemia/reperfusion injury [13].…”

Section: Discussionmentioning

confidence: 99%

Tectorigenin ameliorates myocardial cell injury caused by hypoxia/reoxygenation by inhibiting autophagy via activation of PI3K/AKT/mTOR pathway

Wu¹,

Zhou²,

Guo³

et al. 2022

Trop. J. Pharm Res

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Purpose: To investigate the protective role of tectorigenin in myocardial ischaemia/reperfusion. Methods: Myocardial cells (H9c2) were treated with different concentrations of tectorigenin and exposed to hypoxia/reoxygenation. Cell viability and apoptosis were determined by MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide) and TUNEL (terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling) staining, respectively. Oxidative stress and inflammation were evaluated using enzyme-linked immunosorbent assay (ELISA), while autophagy and the underlying mechanisms of action were evaluated by Western blot. Results: Tectorigenin enhanced the proliferative activity of H9c2 under hypoxia/reoxygenation conditions, and significantly reduced the apoptotic activity (p < 0.001) through decrease in Bax and increase in Bcl-2. Tectorigenin also significantly up-regulated SOD (superoxide dismutase) and GSH (glutathione) levels (p < 0.01), and down-regulated MDA (malondialdehyde) and MPO (myeloperoxidase) in hypoxia/reoxygenation-induced H9c2. TNF-α (tumor necrosis factor-α), IL(interleukin)-1β, and IL-6 levels were also inhibited by tectorigenin by down-regulating p-p65. Hypoxia/reoxygenation-induced increase in p62 and decrease in Beclin-1 and LC3-II/LC3-I were reversed by tectorigenin. Protein expressions of p-mTOR, p-AKT, and p-PI3K in hypoxia/reoxygenation-induced H9c2 were elevated by tectorigenin. Conclusion: Tectorigenin exerts anti-oxidant, anti-inflammatory, and anti-autophagic effects on hypoxia/reoxygenation-induced H9c2 through the activation of PI3K/AKT/mTOR pathway, thus suggesting that it is a potential agent for the management of myocardial ischaemia/reperfusion.

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Section: Discussionmentioning

confidence: 99%

Tectorigenin ameliorates myocardial cell injury caused by hypoxia/reoxygenation by inhibiting autophagy via activation of PI3K/AKT/mTOR pathway

Wu¹,

Zhou²,

Guo³

et al. 2022

Trop. J. Pharm Res

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“…However, a significant proportion of these treatments are associated with adverse effects such as bleeding and suboptimal targeting efficiency ( Zhang et al, 2022 ). Additionally, some studies suggest that conventional antiplatelet medications do not markedly improve clinical symptoms ( Li et al, 2021 ). Thus, combining with traditional Chinese medicine may be a promising therapeutic method under virtue of fewer adverse reactions ( Tu et al, 2020 ).…”

Section: Pharmacological Action Of Rg3 In Heart Diseasesmentioning

confidence: 99%

The protective role of ginsenoside Rg3 in heart diseases and mental disorders

Shi,

Luo,

Wei

et al. 2024

Front. Pharmacol.

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Ginsenoside Rg3, a compound derived from Panax ginseng C. A. Mey., is increasingly recognized for its wide range of pharmacological effects. Under the worldwide healthcare challenges posed by heart diseases, Rg3 stands out as a key subject in modern research on Chinese herbal medicine, offering a novel approach to therapy. Mental illnesses are significant contributors to global disease mortality, and there is a well-established correlation between cardiac and psychiatric conditions. This connection is primarily due to dysfunctions in the sympathetic-adrenomedullary system (SAM), the hypothalamic-pituitary-adrenal axis, inflammation, oxidative stress, and brain-derived neurotrophic factor impairment. This review provides an in-depth analysis of Rg3’s therapeutic benefits and its pharmacological actions in treating cardiac and mental health disorders respectively. Highlighting its potential for the management of these conditions, Rg3 emerges as a promising, multifunctional therapeutic agent.

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“…Currently, physicians are following various strategies to tackle the ischemic-reperfusion-induced cardiac damage/mortality like ischemic preconditioning, postconditioning, and administration of Glucose and insulin (10). The latter two phases of cardiac ischemic reperfusion injury are tackled by treating with antiplatelet and anticoagulant therapy (11, 12). Still, there is an urgent need to understand the pathophysiology of cardiac ischemic reperfusion injury to identify new therapeutic avenues to prevent cardiac ischemic reperfusion injury-associated morbidity.…”

Section: Introductionmentioning

confidence: 99%

GCN5L1 regulates glucose and ketone body metabolism during cardiac ischemia-reperfusion injury

Bugga,

Stoner,

Manning

et al. 2024

Preprint

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Ischemic heart diseases are the leading cause of death among cardiovascular diseases. Reperfusion of the ischemic myocardium is the only way to treat IHD. However, reperfusion can damage the ischemic myocardium if it does not happen at the right time. Therefore, understanding the pathophysiology of cardiac ischemic reperfusion injury is essential to identifying new therapeutic targets. We reported the cardioprotective role of GCN5L1 in ex-vivo cardiac ischemic reperfusion injury through the regulation of cytoprotective signaling by reducing oxidative stress. The current study investigated the role of GCN5L1 in in-vivo cardiac ischemic reperfusion injury and in-vitro H/R injury in AC16 cells. The cardiac-specific GCN5L1 KO did not further deteriorate the cardiac function and infarct size. We measured the glucose metabolism-related protein expression among all experimental groups and found that GCN5L1 KO significantly decreases glucose metabolism by PDH phosphorylation. We further evaluated the role of GCN5L1 in in-vitro H/R injury in genetically modified AC16 cells (GCN5L1 KD and overexpressed and control). GCN5L1 KD in AC16 cells promotes phosphorylation of PDH; similarly, overexpression reduces the p-PDH levels. We identified that the regulation of PDH phosphorylation via PDK4/PDP1/PDPR and GCN5L1 regulates the PDK4 expression. We measured the ketone body metabolism related to protein expression in control and KD cells after H/R injury and found the upregulation of ketone body metabolism-related protein expression in KD cells compared to control AC16 cells. Altogether, our in vivo and in vitro studies findings conclude that GCN5L1 is required for glucose metabolism in ischemic reperfusion injury, and in the absence of GCN5L1, ketone body metabolism accomplishes the cardiac energy requirements and prevents I/R induced cardiac damage and infarct size.Graphical AbstractGraphical abstract of the manuscriptAltogether, our results conclude that Cardiomyocyte-specific GCN5L1 KO in-vivo cardiac ischemic reperfusion injury and in-vitro Hypoxia-reoxygenation stress significantly affect glucose metabolism by suppressing glucose metabolism. Cardiac-specific GCN5L1 KO mice in-vivo and knockdown in AC16 cells invitro upregulates the expression of enzymes that are involved in the ketone body metabolism to rescue from in-vivo cardiac ischemic reperfusion injury and invitro H/R stress.

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Antiplatelet Therapy with Integrated Traditional Chinese and Western Medicine for Use in Myocardial Ischemia-Reperfusion Injury: A Review of Clinical Applications and Mechanisms

Cited by 5 publications

References 51 publications

Tectorigenin ameliorates myocardial cell injury caused by hypoxia/reoxygenation by inhibiting autophagy via activation of PI3K/AKT/mTOR pathway

Tectorigenin ameliorates myocardial cell injury caused by hypoxia/reoxygenation by inhibiting autophagy via activation of PI3K/AKT/mTOR pathway

The protective role of ginsenoside Rg3 in heart diseases and mental disorders

GCN5L1 regulates glucose and ketone body metabolism during cardiac ischemia-reperfusion injury

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