17 beta estradiol/inflammation

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17-Beta-estradiol enhanced allodynia of inflammatory temporomandibular joint through upregulation of hippocampal TRPV1 in ovariectomized rats.

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Temporomandibular disorders (TMDs) predominantly affect reproductive female patients, with pain the most frequent complaint. Although estrogens are believed to play important roles in TMD pain, the mechanism underlying modulation of TMD pain by estrogens remains largely unknown. Accumulating

Pro-inflammatory and pro-oxidant properties of the HIV protein Tat in a microglial cell line: attenuation by 17 beta-estradiol.

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Microglia are activated in humans following infection with human immunodeficiency virus (HIV), and brain inflammation is thought to be involved in neuronal injury and dysfunction during HIV infection. Numerous studies indicate a role for the HIV regulatory protein Tat in HIV-related inflammatory and

A comparison of the anti-inflammatory activities of conjugated estrogens and 17-beta estradiol.

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OBJECTIVE Unregulated chronic inflammatory process partly due to an estrogen deficiency may render postmenopausal women vulnerable to degenerative conditions such as arthritis, osteoporosis, atherosclerosis, and Alzheimer's disease. Current confusion regarding therapeutic efficacy of estrogen

17 Beta-estradiol normalizes Toll receptor 4, mitogen activated protein kinases and inflammatory response in epidermal keratinocytes following trauma-hemorrhage.

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Trauma-hemorrhage produces immunodepression in males but not in proestrus females and this difference is due to the presence of high estrogen in proestrus females. Although skin is the largest immunological organ of the body and is considered the first line of defense, no study to-date has examined

17-β estradiol exerts anti-inflammatory effects through activation of Nrf2 in mouse embryonic fibroblasts.

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Several reports indicate crosstalk between the transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2) and estrogen, which has a protective effect in colorectal cancer (CRC). The aim of this study was to investigate the role of Nrf2 signaling in the anti-inflammatory effect of

17-beta-Estradiol decreases p38 MAPK-mediated myocardial inflammation and dysfunction following acute ischemia.

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Understanding the inflammatory response to myocardial ischemia is an important part of achieving the elusive clinical goal of perfect myocardial protection. While it is established that estrogen affects the chronic inflammatory processes of coronary atherosclerosis, the effects of estrogen on acute

Inflammation-induced Gro1 triggers senescence in neuronal progenitors: effects of estradiol.

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BACKGROUND Inflammation has been proposed to contribute to the decline in adult hippocampal neurogenesis. Proinflammatory cytokines activate transcription of chemokine growth-regulated oncogene α (Gro1) in human and murine hippocampal neuronal progenitor cells (NPC). The goal of this study was to

17β-estradiol and inflammation: implications for ischemic stroke.

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Although typically associated with maintenance of female reproductive function, estrogens mediate physiological processes in nearly every body tissue, including the central nervous system. Numerous pre-clinical studies have shown that estrogen, specifically 17-beta-estradiol (17β-E2), protects the

Inhibition of hepatic drug biotransformation by carrageenan-induced inflammation in the rat: effect of sex hormone alterations.

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Following in vivo treatment with carrageenan, sex-related differences in alteration of hepatic drug metabolism were found in the rat. In adult male rats, marked decreases were observed in hepatic 9000 x g supernatant cytochrome P-450 content and in the biotransformation of hexobarbital, aminopyrine,

17 beta-estradiol induced prostatitis in the rat is an autoimmune disease.

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OBJECTIVE Studies suggest that alteration in steroid hormone levels may be one of the factors causing nonbacterial prostatitis (NBP) in rats. We hypothesized that hormonally induced prostatitis in the rat may be an autoimmune disease. Studies were carried out to prove this hypothesis. METHODS We

The anti-inflammatory activity of estrogen in glial cells is regulated by the PKC-anchoring protein RACK-1.

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It has recently been suggested that estrogen inhibits glial activation and the release of neurotoxic mediators. The mechanisms involved in this anti-inflammatory effect are unclear. We found that an nM concentration of 17-beta estradiol inhibits protein kinaseC-betaII translocation induced by

Effect of 17-beta-estradiol and ginsenoside Rg1 on reactive microglia induced by beta-amyloid peptides.

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The reactive microglias induced by 25 micromol of beta-amyloid peptides (Abeta25-35) and/or IFN-gamma can initiate the microglial respiratory burst and release NO, respectively. Oxidative stress and inflammatory function have been implicated in Alzheimer's disease (AD). We showed that 10 micromol

17-Beta estradiol enhances prostaglandin E2 production in human U937-derived macrophages.

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Prostaglandins (PGs) are potent eicosanoid lipid mediators that have been implicated in numerous homeostatic functions and inflammation. Estrogens have been shown to regulate the expression of genes in lipid metabolism in many cellular systems. In this study, the activation of macrophages and the

Estrogen metabolites in the release of inflammatory mediators from human amnion-derived cells.

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OBJECTIVE Human amnion-derived cells have been used as in vitro models to test the release of inflammatory mediators, such as arachidonic acid (AA) and prostaglandin E(2) (PGE(2)). We compared estrogen metabolites for their ability to induce AA release, to influence PGE(2) production and to interact

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

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