Anthocyanin Cyanidin-3-Glucoside Attenuates Platelet Granule Release in Mice Fed High-Fat Diets

ZHOU, Fang-Hang; Deng, Xiujuan; Chen, Yanqiu; Ya, Fuli; Zhang, Xiandan; Song, Fenglin; Li, Dan; Yang, Yan

doi:10.3177/jnsv.63.237

Cited by 19 publications

(17 citation statements)

References 38 publications

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“…12,13 We previously demonstrated that cyanidin-3-O-β-glucoside (Cy-3-g), the major bioactive compound in anthocyanins, inhibited platelet aggregation, activation, granule secretion, and thrombus formation in vitro, and in vivo in both animal and dyslipidemic human subjects. 10,11,14,15 Our in vitro studies also showed that Cy-3-g induced megakaryocyte apoptosis in the human megakaryoblastic Meg-01 cells 16 and promoted apo-ptosis of activated platelet. 17 However, the effective levels of Cy-3-g were determined at a range between 10 to 100 μmol/L.…”

Section: Introductionsupporting

confidence: 62%

Protocatechuic Acid Protects Platelets from Apoptosis via Inhibiting Oxidative Stress-Mediated PI3K/Akt/GSK3β Signaling

Hong

et al. 2021

Thromb Haemost

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Oxidative stress plays crucial roles in initiating platelet apoptosis that facilitates the progression of cardiovascular diseases (CVDs). Protocatechuic acid (PCA), a major metabolite of anthocyanin cyanidin-3-O-β-glucoside (Cy-3-g), exerts cardioprotective effects. However, underlying mechanisms responsible for such effects remain unclear. Here, we investigate the effect of PCA on platelet apoptosis and the underlying mechanisms in vitro. Isolated human platelets were treated with hydrogen peroxide (H2O2) to induce apoptosis with or without pretreatment with PCA. We found that PCA dose-dependently inhibited H2O2-induced platelet apoptosis by decreasing the dissipation of mitochondrial membrane potential, activation of caspase-9 and caspase-3, and decreasing phosphatidylserine exposure. Additionally, the distributions of Bax, Bcl-xL, and cytochrome c mediated by H2O2 in the mitochondria and the cytosol were also modulated by PCA treatment. Moreover, the inhibitory effects of PCA on platelet caspase-3 cleavage and phosphatidylserine exposure were mainly mediated by downregulating PI3K/Akt/GSK3β signaling. Furthermore, PCA dose-dependently decreased reactive oxygen species (ROS) generation and the intracellular Ca2+ concentration in platelets in response to H2O2. N-Acetyl cysteine (NAC), a ROS scavenger, markedly abolished H2O2-stimulated PI3K/Akt/GSK3β signaling, caspase-3 activation, and phosphatidylserine exposure. The combination of NAC and PCA did not show significant additive inhibitory effects on PI3K/Akt/GSK3β signaling and platelet apoptosis. Thus, our results suggest that PCA protects platelets from oxidative stress-induced apoptosis through downregulating ROS-mediated PI3K/Akt/GSK3β signaling, which may be responsible for cardioprotective roles of PCA in CVDs.

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Section: Introductionsupporting

confidence: 62%

Protocatechuic Acid Protects Platelets from Apoptosis via Inhibiting Oxidative Stress-Mediated PI3K/Akt/GSK3β Signaling

Hong

et al. 2021

Thromb Haemost

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“…It has also been demonstrated that C3G significantly ameliorated hyperglycemia and insulin sensitivity in vivo (Tsuda et al, 2003). A recent in vivo study reported that C3G inhibited release of purified platelet granule and protected against CVD and thrombosis (Zhou et al, 2017). Furthermore, it also diminishes blood glucose level and modulates insulin sensitivity in type 2 diabetic mice.…”

Section: Pharmacological Mechanisms Of Anthocyanins In Metabolic Syndmentioning

confidence: 99%

“…It has also been proven that C3G had synergistic effect with acarbose, a inhibitor of α-glucosidase used in the treatment of diabetes. Furthermore, C3G treatment resulted in increased insulin secretion compared with the control diabetic group, and is a potential phytotherapeutic agent for the prevention of diabetes (Zhou et al, 2017).…”

Section: Pharmacological Mechanisms Of Anthocyanins In Metabolic Syndmentioning

confidence: 99%

Anthocyanins in the Management of Metabolic Syndrome: A Pharmacological and Biopharmaceutical Review

et al. 2018

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The term “metabolic syndrome” (MetS) refers to a combination of diabetes, high blood pressure, and obesity. The origin of MetS includes a combination of multiple factors, such as sedentary lifestyle, unhealthy diet choice, and genetic factors. MetS is highly prevalent and adversely affects the general population by elevating risk of cardiovascular complications, organ failure, and much other pathology associated with late-stage diabetes. Anthocyanins (ANTs) are health-promoting bioactive compounds belonging to the flavonoids subclass of polyphenols. Numerous studies have reported the potential therapeutic benefits on MetS syndrome and diabetes from fruits rich in ANTs. This review summarizes the role of several dietary ANTs on preventing and managing MetS as well as the pharmacological mechanisms and biopharmaceutical features of their action. We also discuss potential nanoformulation and encapsulation approaches that may enhance the bioefficacy of ANTs in MetS. Experiments have demonstrated that ANTs may attenuate the symptoms of MetS via improving insulin resistance, impaired glucose tolerance, dyslipidaemia, cholesterol levels, hypertension, blood glucose, protecting β cells, and preventing free radical production. In brief, the intake of ANT-rich supplements should be considered due to their plausible ability for prevention and management of MetS. Additionally, randomized double-blind clinical trials are obligatory for evaluating the bioefficacy and pharmacological mechanisms of ANTs and their pharmaceutical formulations in patients with MetS.

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“…Pigmented rice-derived polyphenols have also shown inhibition of platelet ATP secretion. Zhou et al [63] conducted in vivo trials on mice fed with high-fat diets. The impact of dietary intervention with the anthocyanin cyanidin-3-glucoside (C3G) purified from black rice was investigated.…”

Section: Impact Of Polyphenols On Platelet Aggregationmentioning

confidence: 99%

“…Mice randomly allocated to one of the 3 groups with 20 subjects for each group: control group (normal diet), high-fat diet (HFD group), or an HFD supplemented with C3G Both Decreased platelet activation, serum lipid levels, and inhibits platelet ATP release [63] In vivo Red wine polyphenols (Provinols™) 149 (uniephrectomized male Sprague-Dawley rats)…”

Section: Bothmentioning

confidence: 99%

Polyphenols: Modulators of Platelet Function and Platelet Microparticle Generation?

Nignpense

Chinkwo

Blanchard

et al. 2019

IJMS

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Platelets and platelet microparticles (PMPs) play a key role in the pathophysiology of vascular disorders such as coronary artery disease and stroke. In atherosclerosis, for example, the disruption of the plaque exposes endogenous agonists such as collagen, which activates platelets. Platelet hyper-activation and the high levels of PMPs generated in such situations pose a thrombotic risk that can lead to strokes or myocardial infarctions. Interestingly, dietary polyphenols are gaining much attention due to their potential to mimic the antiplatelet activity of treatment drugs such as aspirin and clopidogrel that target the glycoprotein VI (GPVI)–collagen and cyclooxygenease-1 (COX-1)–thromboxane platelet activation pathways respectively. Platelet function tests such as aggregometry and flow cytometry used to monitor the efficacy of antiplatelet drugs can also be used to assess the antiplatelet potential of dietary polyphenols. Despite the low bioavailability of polyphenols, several in vitro and dietary intervention studies have reported antiplatelet effects of polyphenols. This review presents a summary of platelet function in terms of aggregation, secretion, activation marker expression, and PMP release. Furthermore, the review will critically evaluate studies demonstrating the impact of polyphenols on aggregation and PMP release.

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Anthocyanin Cyanidin-3-Glucoside Attenuates Platelet Granule Release in Mice Fed High-Fat Diets

Cited by 19 publications

References 38 publications

Protocatechuic Acid Protects Platelets from Apoptosis via Inhibiting Oxidative Stress-Mediated PI3K/Akt/GSK3β Signaling

Protocatechuic Acid Protects Platelets from Apoptosis via Inhibiting Oxidative Stress-Mediated PI3K/Akt/GSK3β Signaling

Anthocyanins in the Management of Metabolic Syndrome: A Pharmacological and Biopharmaceutical Review

Polyphenols: Modulators of Platelet Function and Platelet Microparticle Generation?

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