IMR Press / JIN / Volume 18 / Issue 4 / DOI: 10.31083/j.jin.2019.04.1172
Open Access Original Research
Contrasting effects of acute and long-term corticosterone treatment on amyloid-β, beta-secretase 1 expression, and nuclear factor kappa B nuclear translocation
Show Less
1 Yunnan University, School of Medicine, 2 Cuihu North Road, Kunming, Yunnan 650091, P. R. China
*Correspondence: (Hongkun Bao); (Jing Du)
These authors contributed equally.
J. Integr. Neurosci. 2019, 18(4), 393–400;
Submitted: 29 August 2019 | Accepted: 19 November 2019 | Published: 30 December 2019
Copyright: © 2019 Hou et al. Published by IMR Press.
This is an open access article under the CC BY 4.0 license

Regulation of neuroinflammation is critical to control the detrimental impact of chronic stress in the central nervous system. Neuroinflammation occurs in response to chronic stress, leading to enhanced neuronal damage in the brain. We investigated the regulatory effects of stress hormone corticosterone on neuroinflammation regulator, as well as amyloid-β and Beta-secretase 1related signaling. We demonstrate that corticosterone can both positively and negatively regulate amyloid-β expression, which may be related to the ratio of neuroinflammation regulator and Beta-secretase 1 signaling in rat primary cortical neurons. Thirty minutes of treatment with 1μM corticosterone significantly decreased the nuclear translocation of neuroinflammation mediator neuroinflammation regulator (Western Blot: P < 0.05, Immunofluorescence: P < 0.001) and production of Beta-secretase 1 enzyme (P < 0.01), which was accompanied by a reduction in amyloid-β1-42 levels (P < 0.01). In contrast, 1 µM corticosterone treatment over 3 days increased nuclear neuroinflammation regulator localization (P < 0.001), followed by the upregulation of Beta-secretase 1 (P < 0.01) and amyloid-β1-42 (P < 0.05) expression. This work is the first to demonstrate that the duration of corticosterone exposure can promote or inhibit amyloid-β production, and to link this effect with Beta-secretase 1 / neuroinflammation regulator signaling, together with providing valuable insight into the mechanisms of neuroinflammation and neuroprotection.

beta-secretase 1
nuclear factor kappa B p65
western blot
Figure 1.
Back to top