Akademik Veri Yönetim Sistemi
15th NATIONAL – 1 st INTERNATIONAL CONGRESS OF HISTOLOGY AND EMBRYOLOGY, 26 - 28 Mayıs 2022, ss.54
Introduction: NLRP3 (NLR Family Pyrin Domain Containing 3) inflammasome has been implicated in a
neurodegenerative diseases. Inhibition of NLRP3 inflammasome activation can suppress neuroinflammation, as
a result of which the progression of neurodegenerative diseases can be slowed down. Therefore, we planned an
appropriate treatment strategy to prevent neurodegeneration can inhibit neuroinflammation caused by microglial
activation. Purpose: The aim of this study was to investigate the anti-inflammatory effects of galantamine and
wedelolactone on NLRP3 inflammasome activation in LPS (lipopolysaccharide)-activated microglial activation.
In addition, we investigated the potential mechanisms underlying the pharmacological effects of galantamine and
wedelolactone by assessing the response of NF-κB (Nuclear factor kappa B) signaling pathway and NLRP3
inflammasome activation.
Material-Method: In this study, N9 microglial cells were treated with LPS and ATP (Adenosine triphosphate)
induced NLRP3 inflammasome activition. N9 microglial cells were pretreated with galantamine for 24 h, then
treated with LPS for 4 h and wedelolactone 30 min and finally ATP for 1 h. A qRT-PCR and immunostaining
was subsequently performed to measure the levels of IL-1β (Interleukin-1β), caspase-1, NLRP3 and NF-κB.
Results: It was found that galantamine and wedelolactone combined treatment protected microglial cells upon
LPS-induced cell death. Galantamine and wedelolactone treatment inhibited the expression of NF-κB. The levels
of NLRP3, caspase-1, as well as the secretion IL-1β were decreased by combined treatment.
Conclusion: Our results indicated that galantamine and wedelolactone combined treatment could inhibit
inflammatory cytokine production and NLRP3 inflammasome activation in microglia, the underlying mechanism
of which may be related to NF-κB signaling pathway; and should be considered as a therapeutic strategy for
neuroinflammatory diseases.
Keywords: Galantamine, Wedelolactone, Lipopolysaccharide, Microglia, NLRP3 inflammasome, NF-κB