GW25-e1437 Protective Effect of Tanshinone IIA through the Rho/Rho kinase system on oxidative stress injured human umbilical vein endothelial cell

AbstractEndothelial cell dysfunction is considered a major cause of vascular complications in diabetes. In the present study, we investigated the protective effect of daidzein, a natural isoflavonoid, against high-glucose–induced oxidative damage in human umbilical vein endothelial cells (HUVECs). Treatment with a high concentration of glucose (30 mM) induced oxidative stress in the endothelial cells, against which daidzein protected the cells as demonstrated by significantly increased cell viability. In addition, lipid peroxidation, intracellular reactive oxygen species (ROS) generation, and indirect nitric oxide levels induced by the high glucose treatment were significantly reduced in the presence of daidzein (0.02–0.1 mM) in a dose-dependent manner. High glucose levels induced the overexpression of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and NF-κB proteins in HUVECs, which was suppressed by treatment with 0.04 mM daidzein. These findings indicate the potential of daidzein to reduce high glucose-induced oxidative stress.

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Resveratrol protects against oxidized low-density lipoprotein-induced human umbilical vein endothelial cell apoptosis via inhibition of mitochondrial-derived oxidative stress

Molecular Medicine Reports ◽

10.3892/mmr.2017.6304 ◽

2017 ◽

Vol 15 (5) ◽

pp. 2457-2464 ◽

Cited By ~ 7

Author(s):

Yujie Liu ◽

Xizhou Chen ◽

Jie Li

Keyword(s):

Oxidative Stress ◽

Endothelial Cell ◽

Cell Apoptosis ◽

Umbilical Vein ◽

Low Density Lipoprotein ◽

Density Lipoprotein ◽

Low Density ◽

Oxidized Low Density Lipoprotein ◽

Endothelial Cell Apoptosis ◽

Human Umbilical Vein

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Tanshinone IIA Attenuates H2O2-Induced Injury in Human Umbilical Vein Endothelial Cells

The American Journal of Chinese Medicine ◽

10.1142/s0192415x12500966 ◽

2012 ◽

Vol 40 (06) ◽

pp. 1307-1319 ◽

Cited By ~ 15

Author(s):

Paul Chan ◽

Yen-Cheng Chen ◽

Li-Jen Lin ◽

Tzu-Hurng Cheng ◽

Kazunori Anzai ◽

...

Keyword(s):

Endothelial Cells ◽

Endothelial Cell ◽

Protective Effect ◽

Cell Apoptosis ◽

Caspase 3 ◽

Umbilical Vein ◽

Tanshinone Iia ◽

Cardiovascular Disorders ◽

P53 Expression ◽

Umbilical Vein Endothelial Cells

The injury of endothelial cell is the critical event of vascular disease. In endothelial cell, oxidative stress is regarded as critical to pathogenic factors in endothelial cell injury and apoptosis. Tanshinone IIA is the main effective component of Salvia miltiorrhiza known as "Danshen" in traditional Chinese medicine for treating cardiovascular disorders, but the mechanism by which it exerts the protective effect is not well established. The present study was designed to test the hypothesis that tanshinone IIA can inhibit hydrogen peroxide ( H2O2 )-induced injury and unravel its intracellular mechanism in human umbilical vein endothelial cells (HUVECs). In this study, HUVECs were treated with tanshinone IIA in the presence/absence of H2O2 . The protective effects of tanshinone IIA against H2O2 were evaluated. Our results show that HUVECs incubated with 200 μM H2O2 had significantly decreased the viability of endothelial cells, which was accompanied with apparent cell apoptosis, the activation of caspase-3 and the upregulation of p53 expression, which was known to play a key role in H2O2 -induced cell apoptosis. However, pretreatment with tanshinone IIA (3–10 μM) resulted in a significant resistance to H2O2 -induced apoptosis. In addition, pretreatment with tanshinone IIA decreased the activity of caspase-3 and p53 expression. Tanshinone IIA also induced activating transcription factor (ATF) 3 expression; while knockdown of ATF-3 with ATF-3 siRNAsignificantly reduced tanshinone IIA's protective effect. In conclusion, the present study shows that tanshinone IIA can protect endothelial cells against oxidative injury induced by H2O2 , suggesting that this compound may constitute a promising intervention against cardiovascular disorders and ATF-3 may play an important role in this process.

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VGLL4 Protects against Oxidized-LDL-Induced Endothelial Cell Dysfunction and Inflammation by Activating Hippo-YAP/TEAD1 Signaling Pathway

Mediators of Inflammation ◽

10.1155/2020/8292173 ◽

2020 ◽

Vol 2020 ◽

pp. 1-9

Author(s):

Kaicheng Xu ◽

Haomin Zhao ◽

Xiaolei Qiu ◽

Xiwen Liu ◽

Fucheng Zhao ◽

...

Keyword(s):

Oxidative Stress ◽

Endothelial Cells ◽

Endothelial Cell ◽

Signaling Pathway ◽

Umbilical Vein ◽

Oxidized Ldl ◽

Endothelial Cell Dysfunction ◽

Human Umbilical Vein ◽

Cell Dysfunction ◽

Umbilical Vein Endothelial Cells

Vestigial-like 4 (VGLL4) has been found to have multiple functions in tumor development; however, its role in cardiovascular disease is unknown. The aim of this study was to investigate the effect of VGLL4 on the dysfunction and inflammatory response of Ox-LDL-induced human umbilical vein endothelial cells (HUVECs) and its mechanism, so as to provide a new theoretical basis for the diagnosis and treatment of atherosclerosis. In the present study, the protective activity of VGLL4 inhibiting Ox-LDL-induced apoptosis, oxidative stress, inflammation, and injury as well as its molecular mechanisms was examined using human umbilical vein endothelial cells (HUVECs). The results showed that the expression of VGLL4 was decreased with the increase of Ox-LDL concentration in HUVECs. In addition, the functional study found that VGLL4 overexpression alleviated Ox-LDL-induced oxidative stress, inflammation, and dysfunction and inhibited apoptosis. Further research found that VGLL4 regulated Hippo-YAP/TEAD1 signaling pathway, and the Hippo-YAP/TEAD1 signaling pathway was involved in the protective mechanism of VGLL4 on HUVECs. In conclusion, it suggests that VGLL4 protects against oxidized-LDL-induced endothelial cell dysfunction by activating the Hippo-YAP/TEAD1 signaling pathway.

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