Open AccessAntimalarial Drug Artemisinin Extenuates Amyloidogenesis and Neuroinflammation in APP swe/ PS 1dE9 Transgenic Mice via Inhibition of Nuclear Factor‐κ B and NLRP 3 Inflammasome Activation
Author(s) -
Shi JianQuan,
Zhang ChuChu,
Sun XiuLan,
Cheng XinXin,
Wang JiangBo,
Zhang YingDong,
Xu Jun,
Zou HaiQiang
Publication year - 2013
Publication title -
cns neuroscience and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.403
H-Index - 69
eISSN - 1755-5949
pISSN - 1755-5930
DOI - 10.1111/cns.12066
Subject(s) - inflammasome , neuroinflammation , artemisinin , pharmacology , in vivo , chemistry , inflammation , medicine , immunology , receptor , biology , biochemistry , plasmodium falciparum , microbiology and biotechnology , malaria
Summary Background The activation of nuclear factor‐kappa B ( NF ‐κB) and NLRP 3 inflammasome is involved in neuroinflammation, which is closely linked to A lzheimer's disease ( AD ). In vivo and in vitro studies have suggested that artemisinin shows antiinflammatory effects in inflammation‐related diseases. However, the impacts of artemisinin on AD have not been investigated. Aims In this study, 5‐month‐old APP swe/ PS 1dE9 transgenic mice were treated daily with 40 mg/kg artemisinin for 30 days by intraperitoneal injection to evaluate the effects of artemisinin on AD . Results We found that artemisinin treatment (1) decreased neuritic plaque burden; (2) did not alter Aβ transport across the blood–brain barrier; (3) regulated APP processing via inhibiting β‐secretase activity; (4) inhibited NF ‐κB activity and NALP 3 inflammasome activation in APP swe/ PS 1dE9 double transgenic mice. Conclusions The in vivo study clearly demonstrates that artemisinin has protective effects on AD pathology due to its effects on suppressing NF ‐κB activity and NALP 3 inflammasome activation. Our study suggests that targeting NF ‐κB activity and NALP 3 inflammasome activation offers a valuable intervention for AD .