GLORIA

GEOMAR Library Ocean Research Information Access

Ihre E-Mail wurde erfolgreich gesendet. Bitte prüfen Sie Ihren Maileingang.

Leider ist ein Fehler beim E-Mail-Versand aufgetreten. Bitte versuchen Sie es erneut.

Vorgang fortführen?

Exportieren
Filter
  • Wiley  (3)
  • Xu, Jin  (3)
Materialart
Verlag/Herausgeber
  • Wiley  (3)
Sprache
Erscheinungszeitraum
  • 1
    In: The Anatomical Record, Wiley, Vol. 305, No. 2 ( 2022-02), p. 254-264
    Kurzfassung: Bilirubin encephalopathy (BE) is a neurological syndrome in newborns, mainly caused by neuronal injury due to excessive oxidative stress produced by unconjugated bilirubin (UCB). Neuroglobin (NGB) can protect the brain by removing oxidative stress species, but its expression and significance in BE are not clear. To address this question, the neonatal BE model was established by injecting UCB into the cerebellomedullary cistern of 7‐day‐old SD rats. Rats were divided into a sham and BE 6 hr group, BE 12 hr group, BE 24 hr group, and BE 7 d group according to UCB action times. Hematoxylin/eosin and Nissl staining, and electron microscopy were employed to observe the pathological and ultrastructural changes of nerve cells in each group. Immunofluorescence staining was used to detect NGB expression sites and cell types. Western blotting and quantitative PCR served to detect NGB expression and test the mitochondrial apoptosis signal pathway. The results confirm that UCB can lead to pathological damage and ultrastructural changes in rats' temporal cortex, increasing the expression of apoptosis‐related proteins Bax, Bcl‐2, Cyt c, Caspase‐3, and neuronal NGB. UCB promotes NGB expression with an increase in action time and reach a peak at 12 hr. In summary, brain damage induced by UCB will cause an increase in NGB expression, the increasing NGB can inhibit neuron apoptosis in early BE phases. Therefore, promoting the expression of endogenous NGB, to act as a neuroprotective agent may be a potential treatment strategy for BE.
    Materialart: Online-Ressource
    ISSN: 1932-8486 , 1932-8494
    URL: Issue
    Sprache: Englisch
    Verlag: Wiley
    Publikationsdatum: 2022
    ZDB Id: 2273240-8
    ZDB Id: 2109216-3
    SSG: 12
    Standort Signatur Einschränkungen Verfügbarkeit
    BibTip Andere fanden auch interessant ...
  • 2
    In: The Anatomical Record, Wiley, Vol. 302, No. 2 ( 2019-02), p. 332-338
    Kurzfassung: Curcumin is a natural product with several anti‐Alzheimer's disease (AD) neuroprotective properties. This study aimed to investigate the effects of curcumin on memory deficits, lactate content, and monocarboxylate transporter 2 (MCT2) in APP/PS1 mouse model of AD. APP/PS1 transgenic mice and wild‐type (WT) C57BL/6J mice were used in the present study. Spatial learning and memory of the mice was detected using Morris water‐maze test. Cerebral cortex and hippocampus lactate contents were detected using lactate assay. MCT2 expression in the cerebral cortex and hippocampus was examined by immunohistochemistry and Western blotting. Results showed that spatial learning and memory deficits were improved in curcumin‐treated APP/PS1 mouse group compared with those in APP/PS1 mice group. Brain lactate content and MCT2 protein level were increased in curcumin‐treated APP/PS1 mice than in APP/PS1 mice. In summary, our findings indicate that curcumin could ameliorate memory impairments in APP/PS1 mouse model of AD. This phenomenon may be at least partially due to its improving effect on the lactate content and MCT2 protein expression in the brain. Anat Rec, 302:332–338, 2019. © 2018 Wiley Periodicals, Inc.
    Materialart: Online-Ressource
    ISSN: 1932-8486 , 1932-8494
    URL: Issue
    Sprache: Englisch
    Verlag: Wiley
    Publikationsdatum: 2019
    ZDB Id: 2273240-8
    ZDB Id: 2109216-3
    SSG: 12
    Standort Signatur Einschränkungen Verfügbarkeit
    BibTip Andere fanden auch interessant ...
  • 3
    In: The Anatomical Record, Wiley, Vol. 298, No. 3 ( 2015-03), p. 554-561
    Kurzfassung: Brain edema formation following intracerebral hemorrhage (ICH) appears to be related with aquaporin‐4 (AQP4), which is critically involved in brain volume homeostasis and water balance. Despite its importance, the regulation of AQP4 expression involved in transmembrane water movements still remains rudimentary. Many studies suggest that the internalization of several membrane‐bound proteins, including AQP4, may occur with or without lysosomal degradation. Previously, we investigated the internalization of AQP4 in retinal ischemic‐reperfusion model. Here, we test the hypothesis that AQP4 is internalized post‐ICH and then degraded in the lysosome. The results demonstrated that both AQP4 and the mannose‐6‐phosphate receptor (MPR) co‐localized in perihematomal region at 6 hr post‐ICH. In addition, AQP4 and lysosomal‐associated membrane protein 1 (LAMP1) also co‐localized in perihematomal region, with co‐expression increasing followed by a gradual decrease at different time windows post‐ICH (6, 12, 24, 48, and 72 hr). After ICH, the Evans blue leakage happened very early at 1 hr and the brain swelling occurred at 3 hr. Moreover, we also found the AQP4 mRNA and AQP4 protein were increased post‐ICH. These results suggest that AQP4 is internalized and the lysosome is involved in degrading the internalized AQP4 post‐ICH. Both the AQP4 internalization and lysosomal degradation may provide biophysical insights regarding the potential of new treatments for brain edema. Anat Rec, 298:554–561, 2015. © 2014 Wiley Periodicals, Inc.
    Materialart: Online-Ressource
    ISSN: 1932-8486 , 1932-8494
    URL: Issue
    Sprache: Englisch
    Verlag: Wiley
    Publikationsdatum: 2015
    ZDB Id: 2273240-8
    ZDB Id: 2109216-3
    SSG: 12
    Standort Signatur Einschränkungen Verfügbarkeit
    BibTip Andere fanden auch interessant ...
Schließen ⊗
Diese Webseite nutzt Cookies und das Analyse-Tool Matomo. Weitere Informationen finden Sie hier...