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Estrogen rapid effects:a window of opportunity for the aging brain?

Neural Regeneration Research 2022年第8期17卷 1629-1632页

作者： Ivanny Marchant Jana Stojanova Lilian Acevedo Pablo Olivero Laboratorio de Modelamiento en Medicina Escuela de MedicinaUniversidad de ValparaísoViña del MarChile Interdisciplinary Centre for Health Studies(CIESAL) Universidad de ValparaísoViña del MarChile Servicio de Neurología Hospital Carlos van Buren ValparaísoChile Laboratorio de Estructura y Función Celular Escuela de MedicinaFacultad de MedicinaUniversidad de ValparaísoValparaísoChile Centro Interoperativo en Ciencias Odontológicas y Médicas Universidad de ValparaísoValparaísoChile

Estrogen produces several beneficial effects in healthy neurological tissues and exhibits cardioprotective *** therapy has been widely used to treat menopausal estrogen deficiency for more than 80 *** high initial expectations of cardioprotective effects,there has been substantial distrust following important randomized clinical trials,such as the Women’s Health ***,the timing of treatment in relation to the onset of menopause came under consideration and led to the proposal of the timing hypothesis,that early initial treatment is important,and benefits are lost as the timing since menopause becomes *** analyses of the Women’s Health Initiative data,together with more recent data from randomized and observational trials,consistently show reductions in coronary heart disease and mortality in younger menopausal *** cognitive function,the timing hypothesis is consistent with observations from basic and animal *** is some clinical evidence to support the benefits of hormonal therapy in this context,though skepticism remains due to the paucity of clinical trials of substantial length in younger menopausal *** is likely that the effects of estrogens on cognitive performance are due to rapid mechanisms,including mechanisms that influence Ca2+homeostasis dynamics,provide protection in a hostile environment and reduce inflammatory signals from neural *** the future,inflammatory profiles accounting for early signs of pathological inflammation might help identify the‘window of opportunity’to use estrogen therapy for successful cognitive protection.

关键词： aging cardiovascular prevention cognitive function estrogen hormone treatment inflammaging rapid effects timing hypothesis TRPV1 window of opportunity

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Corticosterone activates Erk1/2 mitogen-activated protein kinase in primary hippocampal cells through rapid nongenomic mechanism

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Progress in Natural Science:Materials International 2005年第4期 38-43页

作者： QI Aiqun 1, QIU Jian 1, XIAO Lin 2 and CHEN Yizhang 2,3 *(1. Department of Physiology, Second Military Medical University, Shanghai 200433, China 2. Department of Neurobiology, Second Military Medical University, Shanghai 200433, China 3. Institute of Neuroscience, Second Military Medical University, Shanghai 200433, China)

Nongenomic effects of glucocorticoids (GC) in various cell types have been well documented, but it still remains unknown whether the mechanism also works in hippocampus which is a crucial target of glucocorticoids in neural system during physiological and/or pathophysiological processes. We present here that corticosterone (B) could rapidly activate Erk1/2 mitogen activated protein kinase (MAPK) in primarily cultured hippocampal cells within minutes, with a bell shaped time dependent curve which peaked at 15min and then went down to normal level in 30 min. This activation was blocked by protein kinase C (PKC) inhibitor (G6976), G protein inhibitor (GDPs), and MEK(MAPK/extracellular signal regulated kinase kinase) inhibitor(PD98059), but not by protein kinase A (PKA) inbibitor (H89), tyrosine kinase inhibitor (genistein), and glucocorticoid receptor (GR) antagonist (RU38486). Thus, the rapid activation of Erk1/2 MAPK in primary hippocampal cells induced by B was likely mediated by a G protein coupled receptor (GPCR) pathway with involvement of PKC, which belonged to the nongenomic rather than genomic mechanism of GC's effects.

关键词： glucocorticoid MAPK rapid effects nongenomic mechanism.

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