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European journal of pharmacology, 2021-12, Vol.913, p.174642-174642, Article 174642
2021
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Autor(en) / Beteiligte
Titel
17β-Estradiol promotes angiogenesis of stria vascular in cochlea of C57BL/6J mice
Ist Teil von
  • European journal of pharmacology, 2021-12, Vol.913, p.174642-174642, Article 174642
Ort / Verlag
Netherlands: Elsevier B.V
Erscheinungsjahr
2021
Quelle
MEDLINE
Beschreibungen/Notizen
  • It is widely accepted that the stria vascularis (SV) in cochlea plays a critical role in the generation of endocochlear potential (EP) and the secretion of the endolymph. 17β-estradiol (E2) is the most potent and abundant endogenous estrogen during the premenopausal period, thus, considered as the reference estrogen. This study aimd to investigate the protective effect of E2 by promoting the expression of vascular endothelial growth factor (VEGF) and thus promoting the vascular regeneration of the SV in elderly mice. After being treated with E2 either in vivo or in vitro, the hearing threshold changes of C57BL/6J elder mice continuously reduced, endothelial cell morphology improved, the number of endothelial cells (ECs) tubular nodes increased significantly, the ability of tubular formation enhanced significantly and the expression of VEGF increased. In vitro, cell model in conjunction with in vivo ovariectomized model was established to demonstrate for the first time that E2 promotes angiogenesis by promoting the secretion of VEGF through the phosphatidylinositol 3-kinase (PI3K)/AKT pathway (PI3K/AKT). In conclusion, E2 demonstrated potent angiogenesis properties with significant protection against Age-Related Hearing Loss (ARHL), which provides a new idea for the improvement of ARHL. •17β-estradiol (E2) plays a role in protecting Age-Related Hearing Loss(ARHL).•Angiogenesis effect of E2 were evaluated.•E2 promote the vascular regeneration of the cochlear stria vascular network in elderly C57BL/6J mice.•E2 promoted VEGF expression was increased in endothelial cells. E2 triggered activation of the PI3K/Akt pathway inducing vascular regeneration.

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