Activity of myricetin and other plant-derived polyhydroxyl compounds in human LDL and human vascular endothelial cells against oxidative stress

Bertin, Riccardo; Chen, Zheng; Marin, Raffaella; Donati, Maddalena; Feltrinelli, Angela; Montopoli, Monica; Zambon, Sabina; Manzato, Enzo; Froldi, Guglielmina

doi:10.1016/j.biopha.2016.05.019

Cited by 40 publications

(20 citation statements)

References 26 publications

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“…Our results demonstrated that myricetin decreased lipid peroxidation in HUVECs in high glucose condition. In agreement with our current data, previous reports have also shown that myricetin decreased MDA production against hydrogen peroxide‐induced stress in cultured HUVECs …”

Section: Discussionsupporting

confidence: 93%

Myricetin ameliorates high glucose‐induced endothelial dysfunction in human umbilical vein endothelial cells

Aminzadeh

Bashiri

2019

Cell Biochemistry & Function

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Endothelial dysfunction is recognized as the initial detectable stage of cardiovascular disease, a serious complication of diabetes. In this study, we evaluated effects of myricetin on high glucose (HG)-elicited oxidative damage in human umbilical vein endothelial cells (HUVECs). The cells were pre-incubated with myricetin and then treated with HG to induce apoptosis. The effect of myricetin on viability was investigated by MTT assay. The levels of lipid peroxidation (LPO) were determined by thiobarbituric acid (TBA) method. The protein expression of Bax, Bcl-2 and caspase-3 was measured by western blot analysis. Moreover, the effect of myricetin on total antioxidant capacity (TAC) and total thiol molecules was also determined.Our results showed that myricetin was able to markedly restore the viability of endothelial cells under oxidative stress. Myricetin reduced HG-caused increase in LPO levels. Also, TAC and total thiol molecules were notably elevated by myricetin.Incubation with myricetin decreased the protein expression levels of Bax, whereas it increased the expression levels of the Bcl-2, compared with HG treatment alone.Furthermore, myricetin significantly decreased cleaved caspase-3 protein expression. It is concluded that myricetin may protect HUVECs from oxidative stress induced by HG via increasing cell TAC and reducing Bax/Bcl-2 protein ratio, and caspase-3 expression.

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Section: Discussionsupporting

confidence: 93%

Myricetin ameliorates high glucose‐induced endothelial dysfunction in human umbilical vein endothelial cells

Aminzadeh

Bashiri

2019

Cell Biochemistry & Function

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“…Magnolol is known to act as an anti-oxidant compound 23 , 24 which would at least partially explain the observed inhibitory effects. Thus, we investigated as to whether Magnolol would decrease the levels of ROS produced in endothelial cells exposed to biomechanical stretch 25 , 26 . While we observed a reduction in ROS levels upon Magnolol pre-treatment under static conditions (Fig.…”

Section: Resultsmentioning

confidence: 99%

Magnolol inhibits venous remodeling in mice

Kuk

Arnold

Meyer

et al. 2017

Sci Rep

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Due to gravity the venous vasculature in the lower extremities is exposed to elevated pressure levels which may be amplified by obesity or pregnancy. As a consequence, venules dilate and may be slowly transformed into varicose or spider veins. In fact, chronically elevated venous pressure was sufficient to cause the corkscrew-like enlargement of superficial veins in mice. We hypothesized that biomechanical activation of endothelial cells contributes to this process and investigated the inhibitory capacity of Magnolol in this context – a natural compound that features multiple properties counteracting cellular stress. While Magnolol did not influence endothelial capillary sprout formation, it interfered with proliferation, ERK1/2 activity, gelatinase activity as well as baseline production of reactive oxygen species in these cells or murine veins. The anti-oxidative and anti-proliferative capacity of Magnolol was mediated through stimulation of heme oxygenase-1 expression. Finally, local transdermal application of Magnolol attenuated pressure-mediated development of varicose/spider veins in mice and was accompanied by the absence of proliferating and MMP-2 positive endothelial cells. Collectively, our data identified Magnolol as a potent inhibitor of biomechanically evoked endothelial cell activity during pressure-mediated venous remodeling processes which contribute to the development of varicose and spider veins.

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“…Myricetin is an important component of the human diet, and has been shown to have major iron-chelating and anti-oxidant roles [24]. In addition, it was observed and proven to have multiple biological activities, including anti-oxidant, anti-inflammatory, neuro-protective, anti-diabetic, ant-arthritic, and anticancer activities [24][25][26][27][28][29][30][31][32][33][34]. Therefore, this study was undertaken to check the prophylactic effect of myricetin in cisplatin-induced colon toxicity by blocking colonic damage, an doxidative and inflammatory processes in Wistar rats.…”

Section: Introductionmentioning

confidence: 99%

Myricetin Abrogates Cisplatin-Induced Oxidative Stress, Inflammatory Response, and Goblet Cell Disintegration in Colon of Wistar Rats

Rehman

Rather

2019

Plants

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Cisplatin [cis-diamminedichloroplatinum II] is an extensively prescribed drug in cancer chemotherapy; it is also useful for the treatment of diverse types of malignancies. Conversely, cisplatin is associated with a range of side effects such as nephrotoxicity, hepatotoxicity, gastrointestinal toxicity, and so on. Myricetin (3,5,7-trihydroxy-2-(3,4,5-trihydroxyphenyl)-4chromenone) is a very common natural flavonoid found in fruits, tea, and plants. It has been found to have high-value pharmacological properties and strong health benefits. To examine the role of myricetin in colon toxicity induced by cisplatin, we conducted a concurrent prophylactic study in experimental animals that were treated orally with myricetin for 14 days at two doses—25 and 50 mg/kg of body weight. On the 14th day, a single intraperitoneal injection of cisplatin (7.5 mg/kg body weight) was administered in all groups except control. The effects of myricetin in cisplatin-induced toxicity in the colon were assessed in terms of antioxidant status, phase-II detoxification enzymes, the level of inflammatory markers, and goblet cell disintegration. Myricetin was found to restore the level of all the antioxidant enzymes analyzed in the study. In addition, the compound ameliorated cisplatin-induced lipid peroxidation, increase in xanthine oxidase activity, and phase-II detoxifying enzyme activity. Myricetin also attenuated deteriorative effects induced by cisplatin by regulating the level of molecular markers of inflammation (NF-κB, Nrf-2, IL-6, and TNF-α), restoring Nrf-2 levels, and controlling goblet cell disintegration. The current study reinforces the conclusion that myricetin exerts protection in colon toxicity via up-regulation of inflammatory markers, improving anti-oxidant status, and protecting tissue damage.

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Activity of myricetin and other plant-derived polyhydroxyl compounds in human LDL and human vascular endothelial cells against oxidative stress

Cited by 40 publications

References 26 publications

Myricetin ameliorates high glucose‐induced endothelial dysfunction in human umbilical vein endothelial cells

Myricetin ameliorates high glucose‐induced endothelial dysfunction in human umbilical vein endothelial cells

Magnolol inhibits venous remodeling in mice

Myricetin Abrogates Cisplatin-Induced Oxidative Stress, Inflammatory Response, and Goblet Cell Disintegration in Colon of Wistar Rats

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