Diammonium Glycyrrhizinate Attenuates Aβ 1–42 ‐Induced Neuroinflammation and Regulates MAPK and NF‐κB Pathways In Vitro and In Vivo

Summary Background and purpose 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.