RETRACTED: Phytoestrogen α-zearalanol inhibits homocysteine-induced endothelin-1 expression and oxidative stress in human umbilical vein endothelial cells

Duan, Jiaqi; Xu, Honghao; Dai, Shunling; Wang, Xiaoming; Wu, Yuwei; Zhang, Yandong; Sun, Renyu; Ren, Jun

doi:10.1016/j.atherosclerosis.2007.08.018

Cited by 22 publications

(17 citation statements)

References 17 publications

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“…Moreover, sustained exposure to the endothelial cells to high levels of Hcy contribute to endothelial dysfunction. 9 ROS oxygen species are known to modulate cellular functions resulting in a diseased cell. Our study suggests that ROS levels are increased in females with unexplained fertility.…”

Section: Discussionmentioning

confidence: 99%

Malondialdehyde and Homocysteine Levels in Patients with Unexplained Female Infertility

Gupta¹,

Chari²

2014

Journal of South Asian Federation of Obstetrics and Gynaecology

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Objectives: To assess association in between malondialdehyde and homocysteine in females with unexplained infertility.Methods: A case control study.Setting: Hospital based.Patients: Fifty females diagnosed with unexplained infertility were matched with fifty normal healthy controls.Intervention: Blood samples for malondialdehyde, a lipid peroxidation product and homocysteine measurements. Results:Our study suggests that females with unexplained infertility have increase in malondialdehyde along with hyperhomocysteinemia when compared with normal healthy controls. Conclusion:Determination of levels of malondialdehyde and homocysteine should be incorporated as one of the factors for ascertaining the cause of female unexplained infertility.

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Section: Discussionmentioning

confidence: 99%

Malondialdehyde and Homocysteine Levels in Patients with Unexplained Female Infertility

Gupta¹,

Chari²

2014

Journal of South Asian Federation of Obstetrics and Gynaecology

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“…There are reports that homocysteine increases inducible NO synthase (iNOS) expression and 3-NT formation in endothelial cells in vitro , and the enhanced nitrative stress plays an important role in homocysteine-induced endothelial dysfunction [8, 9]. Duan et al [29] had reported that α -ZAL may antagonize homocysteine-induced ROS accumulation, which may contribute to α -ZAL-induced beneficial effect on endothelial function. Based on these pieces of work, we further explored whether α -ZAL might inhibit the nitrative stress in homocysteine-treated HUVECs or not.…”

Section: Discussionmentioning

confidence: 99%

Phytoestrogenα-Zearalanol Attenuates Homocysteine-Induced Apoptosis in Human Umbilical Vein Endothelial Cells

Hou

Zhao

et al. 2013

BioMed Research International

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Hyperhomocysteinemia is an independent risk factor for cardiovascular diseases. The enhanced nitrative stress plays an important role in homocysteine-induced endothelial dysfunction. Previous studies have showed that phytoestrogen α-zearalanol alleviated endothelial injury in ovariectomized hyperhomocysteinemic rats; however, the underlying mechanism remains to be clarified. This study was to investigate the effects of α-zearalanol on homocysteine-induced endothelial apoptosis in vitro and explore the possible role of nitrative stress in these effects. Results showed that homocysteine (500 μmol/L, 24 h) induced the apoptosis of human umbilical vein endothelial cells (HUVECs) obviously, and this effect was significantly attenuated by pretreatment with α-zearalanol (10−8~10−6 mol/L). Moreover, α-zearalanol downregulated proapoptotic protein Bax, upregulated antiapoptotic proteins Bcl-2 and Bcl-XL, and decreased the expression and activity of caspase-9. These findings demonstrated that α-zearalanol could effectively alleviate homocysteine-induced endothelial apoptosis, and this antiapoptosis effect might be related to the inhibition of the intrinsic pathway. Western blot indicated an enhanced 3-nitrotyrosine expression in HUVECs when challenged with homocysteine, which was attenuated by pretreatment with α-zearalanol. This result implied that inhibition of nitrative stress might play a role in the protective effect of α-zearalanol on endothelial cells. Such discovery may shed a novel light on the antiatherogenic activities of α-zearalanol in hyperhomocysteinemia.

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“…However, in vascular endothelium, many studies have demonstrated the inhibition of ET-1 expression by estrogens [46,47], a mechanism that may explain the well-known vasoprotective estrogen effects [47].Fulvestrant in contrast to tamoxifen left gene expression of the ET system unaffected, supporting the perception of fulvestrant as the clinically superior compound. Different from the SERM tamoxifen, fulvestrant is an ER antagonist and ER downregulator without agonistic activity [48].…”

Section: Discussionmentioning

confidence: 99%

ETAR antagonist ZD4054 exhibits additive effects with aromatase inhibitors and fulvestrant in breast cancer therapy, and improves in vivo efficacy of anastrozole

Smollich

Götte

Fischgräbe

et al. 2009

Breast Cancer Res Treat

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RETRACTED: Phytoestrogen α-zearalanol inhibits homocysteine-induced endothelin-1 expression and oxidative stress in human umbilical vein endothelial cells

Cited by 22 publications

References 17 publications

Malondialdehyde and Homocysteine Levels in Patients with Unexplained Female Infertility

Malondialdehyde and Homocysteine Levels in Patients with Unexplained Female Infertility

Phytoestrogenα-Zearalanol Attenuates Homocysteine-Induced Apoptosis in Human Umbilical Vein Endothelial Cells

ETAR antagonist ZD4054 exhibits additive effects with aromatase inhibitors and fulvestrant in breast cancer therapy, and improves in vivo efficacy of anastrozole

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