Dihydromyricetin ameliorates foam cell formation via LXRα-ABCA1/ABCG1-dependent cholesterol efflux in macrophages

Zhang, Yi; Peng, Yi; Tang, Kun; Wang, Yu Qin; Zhao, Zhe; Wei, Xinyuan; Xu, Xiao Le

doi:10.1016/j.biopha.2018.02.124

Cited by 45 publications

(28 citation statements)

References 20 publications

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“…Previous research has demonstrated that DMY alleviated myocardial injury and decreased mortality in doxorubicin-induced myocardial injury in mice [ 36 ]. Another study indicated that DMY attenuated atherosclerosis by improving endothelial dysfunction, inhibiting macrophage foam cell formation and ameliorating lipid profiles [ 37 ]. Our previous study found that DMY inhibited Ang II-induced cardiomyocyte hypertrophy and myocardial fibroblast proliferation in vitro [ 17 , 18 ].…”

Section: Discussionmentioning

confidence: 99%

Dihydromyricetin Attenuates Myocardial Hypertrophy Induced by Transverse Aortic Constriction via Oxidative Stress Inhibition and SIRT3 Pathway Enhancement

Chen

Luo

Sun

et al. 2018

IJMS

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Dihydromyricetin (DMY), one of the flavonoids in vine tea, exerts several pharmacological actions. However, it is not clear whether DMY has a protective effect on pressure overload-induced myocardial hypertrophy. In the present study, male C57BL/6 mice aging 8–10 weeks were subjected to transverse aortic constriction (TAC) surgery after 2 weeks of DMY (250 mg/kg/day) intragastric administration. DMY was given for another 2 weeks after surgery. Blood pressure, myocardial structure, cardiomyocyte cross-sectional area, cardiac function, and cardiac index were observed. The level of oxidative stress in the myocardium was assessed with dihydroethidium staining. Our results showed that DMY had no significant effect on the blood pressure. DMY decreased inter ventricular septum and left ventricular posterior wall thickness, relative wall thickness, cardiomyocyte cross-sectional areas, as well as cardiac index after TAC. DMY pretreatment also significantly reduced arterial natriuretic peptide (ANP), brain natriuretic peptide (BNP) mRNA and protein expressions, decreased reactive oxygen species production and malondialdehyde (MDA) level, while increased total antioxidant capacity (T-AOC), activity of superoxide dismutase (SOD), expression of sirtuin 3 (SIRT3), forkhead-box-protein 3a (FOXO3a) and SOD2, and SIRT3 activity in the myocardium of mice after TAC. Taken together, DMY ameliorated TAC induced myocardial hypertrophy in mice related to oxidative stress inhibition and SIRT3 pathway enhancement.

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Section: Discussionmentioning

confidence: 99%

Dihydromyricetin Attenuates Myocardial Hypertrophy Induced by Transverse Aortic Constriction via Oxidative Stress Inhibition and SIRT3 Pathway Enhancement

Chen

Luo

Sun

et al. 2018

IJMS

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“…Luo's found that DMY protects HUVECs from ox‐LDL‐induced oxidative injury by activating Nrf2/HO‐1 pathway by up‐regulating Akt and ERK1/2 . Zeng's study showed that DMY reduce foam cell formation via activation of LXRα‐ABCA1/ABCG1 signalling pathway . Here, we focus on the PI3k/Akt/FoxO3a pathway, which plays crucial role in promoting survival and function of cardiomyocyte.…”

Section: Discussionmentioning

confidence: 93%

Dihydromyricetin protects HUVECs of oxidative damage induced by sodium nitroprusside through activating PI3K/Akt/FoxO3a signalling pathway

Zhang

Wang

et al. 2019

J Cellular Molecular Medi

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The damage of vascular endothelial cells induced by oxidative stress plays an important role in the pathogenesis of atherosclerosis. Dihydromyricetin (DMY) is considered as a natural antioxidant. However, the mechanism of DMY on endothelial cell injury induced by oxidative stress remains unclear. In this study, we found that DMY could reduce the oxidative damage of HUVECs induced by sodium nitroprusside (SNP), HUVECs pre‐treated with DMY suppressed SNP‐induced apoptosis by reduced ROS overproduction of intracellular, decreased MDA level and elevated the superoxide dismutase activity. Meanwhile, we found that DMY could promote the expression of phosphorylated FoxO3a and Akt, and affect the nuclear localization of FoxO3a, when treated with the PI3K inhibitor LY294002, the effect of DMY was blocked. These data suggest that DMY protects HUVECs from oxidative stress by activating PI3K/Akt/FoxO3a signalling pathway. Therefore, DMY may have great therapeutic potential as a new drug for atherosclerosis.

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“…The researchers also confirmed that the enhanced expressions of ABCA1 and ABCG1 by DMY were mediated by liver X receptor α (LXRα) but not peroxisome proliferator-activated receptor-γ (PPARγ). Experiments in vivo also found that DMY attenuated the plaque lesion in aortic root, increased LXRα, ABCA1 and ABCG1 expressions in aorta of the apolipoprotein E (apoE) −/− mice with high fat diet (HFD) ( Zeng Y. et al, 2018 ). The reduced lipid absorbtion but enhanced cholesterol efflux by DMY proposed a great possibility for the prevention or treatment for atherosclerosis.…”

Section: Cardiovascular Systemmentioning

confidence: 99%

Recent Update on the Pharmacological Effects and Mechanisms of Dihydromyricetin

et al. 2018

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As the most abundant natural flavonoid in rattan tea, dihydromyricetin (DMY) has shown a wide range of pharmacological effects. In addition to the general characteristics of flavonoids, DMY has the effects of cardioprotection, anti-diabetes, hepatoprotection, neuroprotection, anti-tumor, and dermatoprotection. DMY was also applied for the treatment of bacterial infection, osteoporosis, asthma, kidney injury, nephrotoxicity and so on. These effects to some extent enrich the understanding about the role of DMY in disease prevention and therapy. However, to date, we still have no outlined knowledge about the detailed mechanism of DMY, which might be related to anti-oxidation and anti-inflammation. And the detailed mechanisms may be associated with several different molecules involved in cellular apoptosis, oxidative stress, and inflammation, such as AMP-activated protein kinase (AMPK), mitogen-activated protein kinase (MAPK), protein kinase B (Akt), nuclear factor-κB (NF-κB), nuclear factor E2-related factor 2 (Nrf2), ATP-binding cassette transporter A1 (ABCA1), peroxisome proliferator-activated receptor-γ (PPARγ) and so on. Here, we summarized the current pharmacological developments of DMY as well as possible mechanisms, aiming to push the understanding about the protective role of DMY as well as its preclinical assessment of novel application.

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Dihydromyricetin ameliorates foam cell formation via LXRα-ABCA1/ABCG1-dependent cholesterol efflux in macrophages

Cited by 45 publications

References 20 publications

Dihydromyricetin Attenuates Myocardial Hypertrophy Induced by Transverse Aortic Constriction via Oxidative Stress Inhibition and SIRT3 Pathway Enhancement

Dihydromyricetin Attenuates Myocardial Hypertrophy Induced by Transverse Aortic Constriction via Oxidative Stress Inhibition and SIRT3 Pathway Enhancement

Dihydromyricetin protects HUVECs of oxidative damage induced by sodium nitroprusside through activating PI3K/Akt/FoxO3a signalling pathway

Recent Update on the Pharmacological Effects and Mechanisms of Dihydromyricetin

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