Abstract

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.

Highlights

  • DMY effectively inhibits tyrosinase activity and reduces melanin amount in cells, attenuates melanoma growth, and protects against ultraviolet A-induced skin damage

  • Our present study found that DMY (20, 40, 80, and 160 μM) pre-administration decreased cell areas, inhibited hypertrophic genes expression, attenuated oxidative stress, enhanced cyclic guanosine monophosphate level and endothelial nitric oxide synthase (NOS) phosphorylation at serine 1177 in angiotensin II (Ang II) induced cardiomyocyte hypertrophy

  • DMY inhibited cell viability and promoted apoptosis in mouse hepatocellular carcinoma Hepal-6 cells, which was associated with reactive oxygen species (ROS) production down-regulation via decreasing transforming growth factor β (TGF-β), Smad3 and nicotinamide adenine dinucleotide phosphate oxidase 4 (NOX4) expression (Liu et al, 2015)

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Summary

Introduction

DMY effectively inhibits tyrosinase activity and reduces melanin amount in cells, attenuates melanoma growth, and protects against ultraviolet A-induced skin damage. DMY enhanced antioxidant capacity, inhibited apoptosis, increased phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) but decreased hypoxia-inducible factor -1α (HIF-1α) expression both in vivo and in vitro (Liu S. et al, 2016). Our present study found that DMY (20, 40, 80, and 160 μM) pre-administration decreased cell areas, inhibited hypertrophic genes expression, attenuated oxidative stress, enhanced cyclic guanosine monophosphate (cGMP) level and endothelial nitric oxide synthase (NOS) phosphorylation at serine 1177 in angiotensin II (Ang II) induced cardiomyocyte hypertrophy.

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