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Silvia Tapia-Gonzalez Instituto Cajal, CSIC, Avenida Doctor Arce 37, E-28002 Madrid, Spain

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Paloma Carrero Instituto Cajal, CSIC, Avenida Doctor Arce 37, E-28002 Madrid, Spain

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Olga Pernia Instituto Cajal, CSIC, Avenida Doctor Arce 37, E-28002 Madrid, Spain

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Luis M Garcia-Segura Instituto Cajal, CSIC, Avenida Doctor Arce 37, E-28002 Madrid, Spain

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Yolanda Diz-Chaves Instituto Cajal, CSIC, Avenida Doctor Arce 37, E-28002 Madrid, Spain

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It has been previously reported that the neuroprotective hormone oestradiol reduces microglia inflammatory activity. The objective of this study was to test whether two selective oestrogen receptor modulators, tamoxifen and raloxifene, modulate in vivo the activation of microglia induced by the peripheral administration of lipopolysaccharide (LPS). Activation of microglia was assessed in the white matter of the cerebellum using immunoreactivity for major histocompatability complex-II. Oestradiol, tamoxifen and raloxifene decreased microglia activation induced by LPS in male and ovariectomized female rats, although the doses of oestradiol that were effective in decreasing microglia reactivity were not the same in both sexes. Tamoxifen reduced microglia activation in all experimental groups at all doses tested (0.5–2 mg/kg b.w.) while raloxifene lost its anti-inflammatory activity at the higher dose tested (2 mg/kg b.w). In addition, raloxifene had per se a moderate pro-inflammatory activity in the brain of control female rats and its anti-inflammatory activity was partially impaired in female animals after 1 month of deprivation of ovarian hormones. Spots of oestrogen receptor (ER)-α immunoreactivity were detected in the soma and cell processes of microglia. Treatment with LPS, oestradiol or tamoxifen induced an increase of ER-α immunoreactive spots in the perikaryon of microglia, while oestradiol antagonized the effect of LPS. The results indicate that some oestrogenic compounds decrease brain inflammation by a mechanism that may involve ERs expressed by microglia. The findings support the potential therapeutic role of oestrogenic compounds as protective anti-inflammatory agents for the central nervous system.

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Yolanda Diz-Chaves Laboratory of Endocrinology, Center for Biomedical Research – CINBIO, University of Vigo, Vigo, Spain
Instituto de Investigación Sanitaria Galicia Sur – IISGS, Vigo, Spain

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Manuel Gil-Lozano Laboratory of Endocrinology, Center for Biomedical Research – CINBIO, University of Vigo, Vigo, Spain
Instituto de Investigación Sanitaria Galicia Sur – IISGS, Vigo, Spain

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Laura Toba Laboratory of Endocrinology, Center for Biomedical Research – CINBIO, University of Vigo, Vigo, Spain
Instituto de Investigación Sanitaria Galicia Sur – IISGS, Vigo, Spain

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Juan Fandiño Laboratory of Endocrinology, Center for Biomedical Research – CINBIO, University of Vigo, Vigo, Spain
Instituto de Investigación Sanitaria Galicia Sur – IISGS, Vigo, Spain

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Hugo Ogando Laboratory of Endocrinology, Center for Biomedical Research – CINBIO, University of Vigo, Vigo, Spain
Instituto de Investigación Sanitaria Galicia Sur – IISGS, Vigo, Spain

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Lucas C González-Matías Laboratory of Endocrinology, Center for Biomedical Research – CINBIO, University of Vigo, Vigo, Spain
Instituto de Investigación Sanitaria Galicia Sur – IISGS, Vigo, Spain

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Federico Mallo Laboratory of Endocrinology, Center for Biomedical Research – CINBIO, University of Vigo, Vigo, Spain
Instituto de Investigación Sanitaria Galicia Sur – IISGS, Vigo, Spain

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Diabetes mellitus exerts metabolic stress on cells and it provokes a chronic increase in the long-term activity of the hypothalamus–pituitary–adrenocortical (HPA) axis, perhaps thereby contributing to insulin resistance. GLP-1 receptor (GLP-1R) agonists are pleiotropic hormones that not only affect glycaemic and metabolic control, but they also produce many other effects including activation of the HPA axis. In fact, several of the most relevant effects of GLP-1 might involve, at least in part, the modulation of the HPA axis. Thus, the anorectic activity of GLP-1 could be mediated by increasing CRF at the hypothalamic level, while its lipolytic effects could imply a local increase in glucocorticoids and glucocorticoid receptor (GC-R) expression in adipose tissue. Indeed, the potent activation of the HPA axis by GLP-1R agonists occurs within the range of therapeutic doses and with a short latency. Interestingly, the interactions of GLP-1 with the HPA axis may underlie most of the effects of GLP-1 on food intake control, glycaemic metabolism, adipose tissue biology and the responses to stress. Moreover, such activity has been observed in animal models (mice and rats), as well as in normal humans and in type I or type II diabetic patients. Accordingly, better understanding of how GLP-1R agonists modulate the activity of the HPA axis in diabetic subjects, especially obese individuals, will be crucial to design new and more efficient therapies for these patients.

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