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Страна 1 од 339 резултати
Genistein suppresses tumor necrosis factor-alpha-induced proliferation via the apoptotic signaling pathway in human aortic smooth muscle cells.
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The proliferation of vascular smooth muscle cells (VSMCs) plays a key role in the development of atherosclerosis. Abnormal VSMC proliferation induces vascular dysfunction and several other pathological processes. The present study investigated the apoptotic effects of genistein on tumor necrosis
The combination of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL/Apo2L) and Genistein is effective in inhibiting pancreatic cancer growth.
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OBJECTIVE
Our previous studies have shown that, contrary to many other human pancreatic adenocarcinoma cell lines, AsPC1 cells are resistant to the apoptotic effect of the tumor necrosis factor-related apoptosis-inducing ligand, also called Apo2L (TRAIL/Apo2L). In our in vitro studies, the
The effect of chronic and acute exercise on thymocyte apoptosis and necrosis in ovariectomized mice given dietary genistein.
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OBJECTIVE
At menopause, many women consume phytoestrogens instead of beginning hormone replacement therapy. Many also start exercise programs for health benefits. Genistein, a soy isoflavone with estrogen-like properties, induces lymphocyte apoptosis in vitro. Aerobic exercise also induces apoptosis
The effects of genistein and puerarin on the activation of nuclear factor-kappaB and the production of tumor necrosis factor-alpha in asthma patients.
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Oxidative stress might play an essential role in the pathogenesis of chronic airway inflammatory diseases, indicating that antioxidant therapy may have a potential effect in controlling chronic airway inflammatory diseases. The aim of the present study was to investigate the effect of antioxidants
[Effects of genistein on interleukin-1beta and tumor necrosis factor-alpha secreted by fibroblast-like synoviocytes isolated from type II collagen-induced arthritis rats].
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OBJECTIVE
To investigate the effects of genistein (Gen) on interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha) secreted by fibroblast-like synoviocytes (FLSs) of rats with type II collagen-induced arthritis (CIA).
METHODS
Type II collagen was injected to induce arthritis in
Isoflavone genistein protects human vascular endothelial cells against tumor necrosis factor-alpha-induced apoptosis through the p38beta mitogen-activated protein kinase.
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Isoflavone genistein may have beneficial effects on vascular function, but the mechanism is unclear. Here, we investigated whether genistein protects vascular endothelial cells against apoptosis induced by tumor necrosis factor-alpha. We show that genistein significantly inhibited TNF-alpha-induced
Genistein reduces tumor necrosis factor alpha-induced plasminogen activator inhibitor-1 transcription but not urokinase expression in human endothelial cells.
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The plasminogen activator inhibitor PAI-1 is markedly elevated in vivo and in vitro upon exposure to the inflammatory mediators tumor necrosis factor alpha (TNF alpha), interleukin-1 (IL-1), and bacterial lipopolysaccharide. Here we report that the isoflavone compound genistein prevents the increase
Effects of resveratrol and genistein on nuclear factor‑κB, tumor necrosis factor‑α and matrix metalloproteinase‑9 in patients with chronic obstructive pulmonary disease.
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Chronic airway inflammation and airway remodeling are the major pathophysiological characteristics of chronic obstructive pulmonary disease (COPD). Resveratrol and genistein have been previously demonstrated to have anti‑inflammatory and antioxidative properties. The present study aimed to measure
Genistein promotes cell death of ethanol-stressed HeLa cells through the continuation of apoptosis or secondary necrosis.
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BACKGROUND
Apoptosis is a major target and treatment effect of multiple chemotherapeutical agents in cancer. A soybean isoflavone, genistein, is a well-studied chemopreventive agent and has been reported to potentiate the anticancer effect of some chemotherapeutics. However, its mechanistic basis of
Genistein suppresses tumor necrosis factor α-induced inflammation via modulating reactive oxygen species/Akt/nuclear factor κB and adenosine monophosphate-activated protein kinase signal pathways in human synoviocyte MH7A cells.
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OBJECTIVE
Genistein, an isoflavone derivative found in soy, is known as a promising treatment for rheumatoid arthritis (RA). However, the detailed molecular mechanism of genistein in suppression of proinflammatory cytokine production remains ambiguous. The aim of this work was to evaluate the signal
Genistein potentiates inhibition of tumor growth by radiation in a prostate cancer orthotopic model.
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OBJECTIVE
We have shown previously that pretreatment with genistein potentiated cell killing induced by radiation in human PC-3 prostate carcinoma cell line in vitro. We tested this approach in vivo using an orthotopic prostate carcinoma model of PC-3 cells in nude mice.
METHODS
Established prostate
Tumor necrosis factor-alpha-induced cyclooxygenase-2 expression in human tracheal smooth muscle cells: involvement of p42/p44 and p38 mitogen-activated protein kinases and nuclear factor-kappaB.
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This study was to determine the mechanism of tumor necrosis factor-alpha (TNF-alpha)-enhanced cyclooxygenase (COX)-2 expression associated with prostaglandin E2 (PGE2) synthesis in human tracheal smooth muscle cells (HTSMCs). TNF-alpha markedly increased COX-2 expression and PGE2 synthesis in a
Infectious spleen and kidney necrosis virus (a fish iridovirus) enters Mandarin fish fry cells via caveola-dependent endocytosis.
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Infectious spleen and kidney necrosis virus (ISKNV) is the type species of the genus Megalocytivirus from the family Iridoviridae. Megalocytiviruses have been implicated in more than 50 fish species infections and currently threaten the aquaculture industry, causing great economic losses in China,
Tumor necrosis factor-alpha activation of the c-Jun N-terminal kinase pathway in human neutrophils. Integrin involvement in a pathway leading from cytoplasmic tyrosine kinases apoptosis.
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The intensity and duration of an inflammatory response depends on the balance of factors that favor perpetuation versus resolution. At sites of inflammation, neutrophils adherent to other cells or matrix components are exposed to tumor necrosis factor-alpha (TNFalpha). Although TNFalpha has been
Genistein and daidzein, typical soy isoflavones, inhibit TNF-α-mediated downregulation of adiponectin expression via different mechanisms in 3T3-L1 adipocytes.
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METHODS
Previous reports suggest that soy isoflavones have multiple biological functions and may help to restore adiponectin expression and insulin sensitivity. However, little is known about whether soy isoflavones can inhibit the downregulation of adiponectin and their molecular mechanisms. In the
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