Anti-thrombotic effects mediated by dihydromyricetin involve both platelet inhibition and endothelial protection

Chen, Shuai; Lv, Keyu; Sharda, Anish V.; Deng, Jun; Zhang, Chao; Hu, Qinghua; Jin, Pengfei; Yao, Guangmin; Xu, Xulin; Ming, Zhang-Yin; Fang, Chao

doi:10.1016/j.phrs.2021.105540

Cited by 26 publications

(32 citation statements)

References 46 publications

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“…Sixty adult patients with nonalcoholic fatty liver disease underwent a randomized double-blind experiment. Following DHM treatment, the level of TNF-α and cytokeratin-18 in serum decreased significantly in this group ( Chen et al, 2021b ). In a randomized double-blind trial of 80 patients with type two diabetes for 1 month, data showed that DHM supplementation significantly improved renal function parameters and glycemic control in patients with type two diabetes mellitus ( Ran et al, 2019 ).…”

Section: Clinical Study Of Dihydromyricetinmentioning

confidence: 92%

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Mechanism of Dihydromyricetin on Inflammatory Diseases

Sun

Yang

et al. 2022

Front. Pharmacol.

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Inflammation plays a crucial role in a variety of diseases, including diabetes, arthritis, asthma, Alzheimer’s disease (AD), acute cerebral stroke, cancer, hypertension, and myocardial ischemia. Therefore, we need to solve the problem urgently for the study of inflammation-related diseases. Dihydromyricetin (DHM) is a flavonoid mainly derived from Nekemias grossedentata (Hand.-Mazz.) J.Wen and Z.L.Nie (N.grossedentata). DHM possesses many pharmacological effects, including anti-inflammatory (NLRP-3, NF-κB, cytokines, and neuroinflammation), antioxidant, improving mitochondrial dysfunction, and regulating autophagy and so on. In this review, we consulted the studies in the recent 20 years and summarized the mechanism of DHM in inflammation-related diseases. In addition, we also introduced the source, chemical structure, chemical properties, and toxicity of DHM in this review. We aim to deepen our understanding of DHM on inflammation-related diseases, clarify the relevant molecular mechanisms, and find out the problems and solutions that need to be solved urgently. Providing new ideas for DHM drug research and development, as well as broaden the horizons of clinical treatment of inflammation-related diseases in this review. Moreover, the failure of clinical transformation of DHM poses a great challenge for DHM as an inflammation related disease.

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Section: Clinical Study Of Dihydromyricetinmentioning

confidence: 92%

“…DHM improved liver function and brain histopathology in mice with acute liver failure related the hepatic encephalopathy ( Cheng et al, 2021 ). In addition, DHM also has anti-thrombotic effects ( Chen et al, 2021a ) ( Figure 3 ).…”

Section: Other Mechanisms Of Dhm Except For Anti-inflammatorymentioning

confidence: 99%

Mechanism of Dihydromyricetin on Inflammatory Diseases

Sun

Yang

et al. 2022

Front. Pharmacol.

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“…Furthermore, fucoidan has been shown to induce angiogenesis in HUVECs through the phosphorylation of MAPKs [ 31 ]. Recent studies have demonstrated that the activation of MAPKs can protect endothelial injury to resist thrombosis [ 34 ]. The results of this study demonstrated that the MAPK signaling was activated in HUVECs.…”

Section: Discussionmentioning

confidence: 99%

Tetramethylpyrazine Protects Endothelial Injury and Antithrombosis via Antioxidant and Antiapoptosis in HUVECs and Zebrafish

Zhang

et al. 2022

Oxidative Medicine and Cellular Longevity

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Chuanxiong Rhizoma, the dried rhizome of Ligusticum chuanxiong Hort., is a commonly used drug for promoting blood circulation and dissipating congestion. Tetramethylpyrazine (TMP), the main active ingredient of Ligusticum chuanxiong, has significant antioxidant, anti-inflammatory, and vascular protective effects. However, the protective properties and underlying mechanisms of TMP against endothelial injury-induced insufficient angiogenesis and thrombosis have not been elucidated. Therefore, we aimed to explore the protective effects of TMP on endothelial injury and its antithrombotic effects and study the mechanism. In vitro experiments showed that TMP could alleviate hydrogen peroxide– (H2O2–) induced endothelial injury of human umbilical vein endothelial cells (HUVECs) and the protective mechanism might be related to the regulation of MAPK signaling pathway, and its antioxidative and antiapoptotic effects. In vivo experiments showed that TMP restored PTK787-induced damage to intersegmental vessels (ISVs) in Tg(fli-1: EGFP)y1 transgenic (Flik) zebrafish larvae. Similarly, adrenalin hydrochloride– (AH–) induced reactive oxygen species (ROS) production and thrombosis in AB strain zebrafish were inhibited by TMP. RT-qPCR assay proved that TMP could inhibit the expression of fga, fgb, fgg, f7, and von Willebrand factor (vWF) mRNA to exert an antithrombotic effect. Our findings suggest that TMP can contribute to endothelial injury protection and antithrombosis by modulating MAPK signaling and attenuating oxidative stress and antiapoptosis.

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“…However, preclinical studies demonstrate that deficiency in platelet ERp57 resulted in increased tail bleeding times and delayed thrombus formation [62]. When compared to quercetin, a flavonoid with a similar chemical structure, the observed effects of myricetin on platelet activation were comparable [63]. Quercetin reduces thrombin-induced platelet aggregation as well as platelet activation via specific agonists of PAR1 and PAR4.…”

Section: Protein Disulfide Isomerasementioning

confidence: 99%

Regulation of Key Antiplatelet Pathways by Bioactive Compounds with Minimal Bleeding Risk

Fuentes

Wehinger

Trostchansky

2021

IJMS

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Cardiovascular disease is strongly influenced by platelet activation. Platelet activation and thrombus formation at atherosclerotic plaque rupture sites is a dynamic process regulated by different signaling networks. Therefore, there are now focused efforts to search for novel bioactive compounds which target receptors and pathways in the platelet activation process while preserving normal hemostatic function. The antiplatelet activity of numerous fruits and vegetables and their multiple mechanisms of action have recently been highlighted. In this review, we review the antiplatelet actions of bioactive compounds via key pathways (protein disulfide isomerase, mitogen-activated protein kinases, mitochondrial function, cyclic adenosine monophosphate, Akt, and shear stress-induced platelet aggregation) with no effects on bleeding time. Therefore, targeting these pathways might lead to the development of effective antiplatelet strategies that do not increase the risk of bleeding.

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Anti-thrombotic effects mediated by dihydromyricetin involve both platelet inhibition and endothelial protection

Cited by 26 publications

References 46 publications

Mechanism of Dihydromyricetin on Inflammatory Diseases

Mechanism of Dihydromyricetin on Inflammatory Diseases

Tetramethylpyrazine Protects Endothelial Injury and Antithrombosis via Antioxidant and Antiapoptosis in HUVECs and Zebrafish

Regulation of Key Antiplatelet Pathways by Bioactive Compounds with Minimal Bleeding Risk

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