17 beta estradiol/nekroos

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17 beta-estradiol inhibits tumor necrosis factor-alpha-induced nuclear factor-kappa B activation by increasing nuclear factor-kappa B p105 level in MCF-7 breast cancer cells.

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Tumor necrosis factor-alpha (TNF-alpha) exerts many cytological effects on a wide range of cells. TNF-alpha can activate nuclear factor-kappa B (NF-kappa B). Activation of NF-kappa B by TNF-alpha mediates many functions of TNF-alpha. The NF-kappa B inhibitor, I kappa B alpha, negatively regulates

Improvement of function and morphology of tumor necrosis factor-alpha treated endothelial cells with 17-beta estradiol: a preliminary study for a feasible simple model for atherosclerosis.

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BACKGROUND Dysfunction of endothelial cells (EC) to produce endothelial nitric oxide synthase (eNOS) by tumor necrosis factor-alpha (TNF-alpha) causes critical features of vascular inflammation associated with several disease states (eg, atherosclerosis including increased platelet aggregation and

Demonstration of tumor necrosis factor-alpha in preovulatory follicular fluid: its association with serum 17 beta-estradiol and progesterone.

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In the present study we have measured the concentrations of interleukin-1 beta (IL-1 beta) and tumor necrosis factor-alpha (TNF-alpha) in preovulatory follicular fluid (FF) samples obtained from patients undergoing ovulation induction with human menopausal gonadotropin/human chorionic gonadotropin.

Production of various cytokines by normal human osteoblast-like cells in response to interleukin-1 beta and tumor necrosis factor-alpha: lack of regulation by 17 beta-estradiol.

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We investigated, in five cell strains per experiment, whether several cytokines known or believed to have effects on bone resorption were produced by nearly homogeneous strains of cultured normal human osteoblast-like (hOB) cells that display virtually the complete phenotype of the mature

17 Beta-estradiol (E2) plus tumor necrosis factor-alpha induces a distorted maturation of human monocyte-derived dendritic cells and promotes their capacity to initiate T-helper 2 responses.

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There is growing evidence that 17 beta-estradiol (E2) modulates immune function. Recent studies indicated that certain effects of E2 on in vivo immune function are not a result of a direct action on T cells, but rather an indirect action on antigen-presenting cells. This study demonstrates that the

17-Beta-estradiol protects the liver against warm ischemia/reperfusion injury and is associated with increased serum nitric oxide and decreased tumor necrosis factor-alpha.

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BACKGROUND Ischemia/reperfusion injury (I/R injury) to the liver can occur in low-flow states associated with trauma and shock and surgical procedures such as liver transplantation. Recent studies have shown that the administration of the female sex hormone 17-beta-estradiol after trauma-hemorrhage

17 Beta-estradiol improves survival in male mice with cardiomyopathy induced by cardiac-specific tumor necrosis factor-alpha overexpression.

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A transgenic mouse model of congestive heart failure (CHF) consequent to cardiac-specific overexpression of tumor necrosis factor-alpha (TNF-alpha) (TNF1.6) displays marked sex-related phenotypic differences. To clarify the potential contributions of estrogen to these sex-specific differences, male

[DEGENERATION AND NECROSIS OF THE LIVER AND KIDNEY IN RATS AFTER THE ADMINISTRATION OF HIGH DOSES OF 17-BETA-ESTRADIOL AND ESTRIOL].

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Effect of tumour necrosis factor-alpha on estrogen metabolic pathways in breast cancer cells.

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Tumor necrosis factor-alpha (TNF-α) is a proinflammatory cytokine that has been linked to breast cancer development. Estrogen metabolic pathway is also involved in breast carcinogenesis and DNA adducts formation. In this study we investigated the effect of TNF-α on the estrogen metabolic pathway in

Preventive effects of withaferin A isolated from the leaves of an Indian medicinal plant Withania somnifera (L.): comparisons with 17-β-estradiol and alendronate.

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OBJECTIVE Bone protective effects of withaferin A (WFA) from leaves of Withania somnifera (L.) were evaluated in preventive model of Balb/c mice with 17 β-estradiol (E2) and alendronate (ALD). METHODS Adult female Balb/c mice, 7 to 9 wk, were bilaterally ovariectomized (OVx) to mimic the state of E2

Protective role of normothermic, hyperthermic and estrogen preconditioning and pretreatment on tumour necrosis factor-alpha-induced damage.

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BACKGROUND Tumour necrosis factor-alpha (TNF-α) has been reported to play an important role in ischemia reperfusion injury and ischemic preconditioning (IPC). However, its role is not completely understood. Recently, normothermic IPC (NIPC), hyperthermic IPC (HIPC), preconditioning (PC) with 17-beta

Protection from myocardial reperfusion injury by acute administration of 17 beta-estradiol.

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Although several studies have demonstrated that chronic exposure to estrogen appears to be cardioprotective, acute circulatory effects of estrogen are largely unknown. Therefore, we studied the effects of acute administration of 17 beta-estradiol in myocardial ischemia/reperfusion. Cats were

[The protective effect of 17 beta-estradiol in experimental myocardial infarct].

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The effect of 17 beta-estradiol on the regions of ischemia and necrosis in experimental myocardial infarction was studied in the experiments on rats. The ability of the hormone to decrease the damaged area due to anti-ischemic and antinecrotic effects is found.

17-β-estradiol inhibits hyperosmolarity-induced proinflammatory cytokine elevation via the p38 MAPK pathway in human corneal epithelial cells.

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OBJECTIVE To evaluate the effects of 17-β-estradiol on hyperosmolar stress-induced proinflammatory cytokine production of interleukin (IL)-6, IL-1, and tumor necrosis factor-alpha (TNF-α) in SV40-immortalized human corneal epithelial cells (hCECs) and the regulatory effects of the mitogen-activated

The role of 17-beta estradiol in ischemic preconditioning protection of the heart.

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BACKGROUND The protective effects of 17-beta estradiol (E2) on cardiac tissue during ischemia/reperfusion (I/R) injury have not yet been fully elucidated. OBJECTIVE To assess the protective effects of short- and long-term E2 treatments on cardiac tissue exposed to I/R, and to assess the effects of

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