alpha-Zearalanol attenuates oxLDL-induced ET-1 gene expression, ET-1 secretion and redox-sensitive intracellular signaling activation in human umbilical vein endothelial cells.

alpha-Zearalanol (alpha-ZAL), a phytochemical with both antioxidant and estrogen-like properties, has been shown to retard progression of atherosclerosis and regulate cardiovascular function in part through suppression of endothelin-1 (ET-1) secretion. However, the precise nature behind alpha-ZAL-elicited inhibition on ET-1 cascade is not largely known. Oxidized low density lipoprotein (oxLDL) plays a critical role in the expression and secretion of ET-1 as well as the onset and progression of atherosclerosis through accumulation of reactive oxygen species (ROS) and activation of mitogen-activated protein kinase stress signaling cascade.

Reactive oxygen species mediate oxidized low-density lipoprotein-induced endothelin-1 gene expression via extracellular signal-regulated kinase in vascular endothelial cells.

Background: Oxidized low-density lipoprotein (oxLDL) promotes expression and secretion of endothelin-1 (ET-1), however, the precise mechanism involved is unclear. This study was designed to identify the regulatory mechanism of oxLDL-induced ET-1 expression in endothelial cells.

Methods: ET-1 mRNA expression, secretion and promoter activity were evaluated by reverse transcriptase-PCR (RT-PCR), enzyme immunometric and luciferase assays, respectively.

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

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[Signaling pathways in expression of inducible nitric oxide synthase induced by high mobility group box 1 in rat alveolar macrophages].

Objective: To explore roles of extracellular signal-regulated kinase (ERK) 1/2, p38 mitogen activated protein kinase (p38 MAPK) and nuclear factor (NF) -KB in expression of inducible nitric oxide synthase (iNOS) in rat alveolar macrophages induced by high mobility group box 1 (HMGB1 ).

Methods: Primary rat alveolar macrophages (PRAMs) cultured in vitro were incubated with PD98059 ( inhibitor against ERK), SB203580 (inhibitor against p38 MAPK) , PDTC (inhibitor against NF-kappaB), or PD98059 plus SB203580 for 2 hours, respectively. HMGB1 was added into the cultures and incubated with cells for 6 hours.

Phytoestrogen alpha-zearalanol antagonizes homocysteine-induced imbalance of nitric oxide/endothelin-1 and apoptosis in human umbilical vein endothelial cells.

Although the issue of estrogen replacement therapy on cardiovascular health is debatable, it has presumable benefits for endothelial function in postmenopausal women. However, the fear of breast cancer has intimidated women contemplating estrogen treatment and limited its long-term application. An effective alternative remedy not associated with breast carcinoma is in serious demand.

Inhibitory effects of alpha-zearalenol on angiotensin II-induced integrin beta3 mRNA via suppression of nuclear factor-kappaB.

Objective: To investigate the effect of alpha-zearalenol on angiotensin II-induced beta3 integrin mRNA expression in human umbilical vein endothelial cells (HUVECs).

Methods: The mRNA level in integrin beta3 was determined by reverse transcription-polymerase chain reaction. Endothelial NF-kappaB activity was determined by the luciferase activity assay of plasmid NF-kappaB-LUC.

Angiotensin II stimulates endothelial integrin beta3 expression via nuclear factor-kappaB activation.

The present study examined the effect and part mechanism of angiotensin II-stimulated integrin beta3 gene expression in human umbilical vein endothelial cells. Protein level and mRNA level of integrin beta3 expression were determined using enzyme-linked immunoadsorbent assay and reverse transcription-polymerase chain reaction. Four plasmids of 5'-different deletion of integrin beta3 gene promoter were constructed to transiently transfected into cells to uncover the region in response to angiotensin II.

TSC-36/FRP inhibits vascular smooth muscle cell proliferation and migration.

Objective: In-stent restenosis is a vascular proliferation/migration disorder characterized by hyperplasia of vascular smooth muscle cells (VSMCs). Because mounting evidence suggests that the therapeutic potential of anti-proliferation and anti-migration therapy, we investigated possible inhibitory effects of the matricellular protein TGF-beta-stimulated clone 36 (TSC-36) on vascular smooth muscle cell proliferation and migration in vitro and in vivo.

Methods: Human umbilical artery smooth muscle cells (SMCs) were treated with inducting agents daidzein or estradiol.

[Cardiovascular effects of phytoestrogens].

Phytoestrogens are bioactive substances existing in natural plants. They have similar molecular structure to those of estrogens. In this article we introduced their classification and sources, and elucidated their effects on heart from aspects involving cardiac function and myocardial electrophysiology.

Phytoestrogen alpha-zearalanol antagonizes oxidized LDL-induced inhibition of nitric oxide production and stimulation of endothelin-1 release in human umbilical vein endothelial cells.

Oxidative modification of low-density lipoprotein (LDL) leads to formation of the atherogenic molecule oxidized LDL (oxLDL), which is considered to be an important mediator for vascular endothelial dysfunction and atherosclerosis. It is speculated that reduced nitric oxide (NO) release/bioavailability and enhanced release of endothelin-1 (ET-1) may contribute to oxLDL-induced endothelial dysfunction. Estrogen may improve lipid profile and inhibit oxLDL-induced endothelial damage.

[Effect of xianzhen tablet on content of advanced glycosylation end products (AGEs) and mRNA expression of AGE-specific cellular receptor in renal cortex of diabetic rats].

Objective: To investigate the effect of Xianzhen tablet (XZT, a Chinese patent compound recipe) on advanced glycosylation end products (AGEs) and mRNA expression of AGE-specific cellular receptor (RAGE) in renal cortex of diabetic rats in order to explore the mechanism of XZT in protecting kidney.

Methods: The diabetic rat model with persistent hyperglycemic renal damage was reproduced by streptozotocin. Fluorescent assay and RT-PCR were used to determine the content of AGEs and expression of RAGE mRNA in renal cortex in model rats, which were treated with XZT and controlled by aminoguanidine (AG) administration.

Roles of NF-kappaB and SP-1 in oxidative stress-mediated induction of platelet-derived growth factor-B by TNFalpha in human endothelial cells.

Platelet-derived growth factor-B (PDGF-B) is upregulated by proinflamatory stimuli in the early stages of atherosclerosis. However, its mechanisms are not fully elucidated. In the present study, by using the antioxidant N-acetylcysteine (NAC), we investigated in human umbilical vein endothelial cells (HUVECs) the roles of oxidative stress in PDGF-B expression induced by tumor necrosis factor alpha (TNFalpha) and its underlying mechanisms.

[Acute lung injury and changes of myocardial ATP enzymes induced by lipopolysaccharide in aging rats].

Objective: To investigate whether acute lung injury (ALI) and changes of myocardial ATP enzymes were induced by intravenous or intraventricle of left heart injection of lipopolysaccharide (LPS) in aging rats.

Methods: 40 male Wistar rats were used for reproducing aging animal model. Aging rats were randomly divided into aging control group (n = 8), ALI group (LPS, 5 mg/kg body weight intravenous injection, n = 16), and LPS group (same dosage LPS, intraventricle of left heart injection, n = 16).

[Hepatic injury induced by acute lung injury in aging rats].

Objective: To investigate the induction of hepatic function damage by acute lung injury (ALI) in aging rats and the effect of Ginkgo Biloba extract (GBE) on this process.

Methods: Thirty male Wistar rats were used to produce the aging animal model. Aging rats were randomly divided into three groups: the control group, the lipopolysaccharide (LPS, intravenous injection) group, and the GBE + LPS group (GBE given 7 days before experiment, once a day, via the esophagus).

[Protective effect of Ginkgo biloba extract on acute lung injury induced by lipopolysaccharide in D-galactose aging rats].

Objective: To investigate the effect of Ginkgo biloba extract (GBE) on acute lung injury(ALI) induced by lipopolysaccharide (LPS) in aging rats.

Methods: The rats were randomly divided into two parts: six rats served as normal controls; 18 rats were used for producing the aging animal model ( D-gal 50 mg/kg body weight was injected intraperitoneally, once a day for 6 weeks). The aging rats were then randomly divided into 3 groups: 6 rats as the aging control group; another 6 as the LPS treated aging group (LPS,5 mg/kg body weight intravenous injection); and the third as the GBE+LPS group (6 rats, GBE was started 7 days before the experiment,given once a day via the esophagus, the amount of flavone glycosides administered being 8 mg/kg body weight, and on the day of experiment, one dose of GBE was given 2 hours before LPS administration ).