In:
CNS Neuroscience & Therapeutics, Wiley, Vol. 19, No. 2 ( 2013-02), p. 117-124
Abstract:
Beta‐amyloid ( A β)‐mediated inflammation contributes to the progression and chronicity of A lzheimer's disease ( AD ), although the exact mechanism remains unclear. This study aimed to investigate whether diammonium glycyrrhizinate ( DG ) could inhibit A β‐induced inflammation in vitro and in vivo and to explore the underlying mechanisms. Methods Aβ 1–42 was injected to bilateral hippocampus of mice to make the AD models in vivo . The levels of m RNA and protein of inflammatory cytokines were measured by real‐time PCR and Western blotting, respectively. The viability of SH ‐ SY 5 Y and HT ‐22 cells was determined by MTT . NF ‐κ B p65 translocation was analyzed by W estern blotting and immunostaining. Phosphorylation of ERK , p38, and JNK was tested by Western blotting. Results DG suppressed A β 1–42 ‐induced activation of microglia and inflammation in vitro and in vivo . The media from A β 1–42 ‐activated microglia decreased the viability of SH ‐ SY 5 Y and HT ‐22 cells, but it was rescued when pretreated with DG . DG could inhibit the activation of MAPK and NF ‐κ B signaling pathways and attenuate the memory deficits in A β 1–42 ‐induced AD mice. Conclusions DG protects A β 1–42 ‐induced AD models in vitro and in vivo through reducing activation of microglia and inflammation, which may be involved in MAPK and NF ‐κ B pathways.
Type of Medium:
Online Resource
ISSN:
1755-5930
,
1755-5949
DOI:
10.1111/cns.2013.19.issue-2
Language:
English
Publisher:
Wiley
Publication Date:
2013
detail.hit.zdb_id:
2423467-9
