Atorvastatin pretreatment attenuates kainic acid-induced hippocampal neuronal death via regulation of lipocalin-2-associated neuroinflammation.
10.4196/kjpp.2018.22.3.301
- Author:
Zhen JIN
1
;
Yohan JUNG
;
Chin ok YI
;
Jong Youl LEE
;
Eun Ae JEONG
;
Jung Eun LEE
;
Ki Jong PARK
;
Oh Young KWON
;
Byeong Hoon LIM
;
Nack Cheon CHOI
;
Gu Seob ROH
Author Information
1. Department of Anatomy and Convergence Medical Science, Institute of Health Sciences, College of Medicine, Gyeongsang National University, Jinju 52727, Korea. anaroh@gnu.ac.kr
- Publication Type:Original Article
- Keywords:
Atorvastatin;
Hippocampal cell death;
Kainic acid;
Lipocalin-2;
Seizures
- MeSH:
Animals;
Atorvastatin Calcium*;
Brain;
Cardiovascular Diseases;
Cell Death;
Cyclooxygenase 2;
Hippocampus;
Hydroxymethylglutaryl-CoA Reductase Inhibitors;
Kainic Acid;
Mice;
Neurons*;
Phosphorylation;
Prevalence;
Seizures
- From:The Korean Journal of Physiology and Pharmacology
2018;22(3):301-309
- CountryRepublic of Korea
- Language:English
-
Abstract:
Statins mediate vascular protection and reduce the prevalence of cardiovascular diseases. Recent work indicates that statins have anticonvulsive effects in the brain; however, little is known about the precise mechanism for its protective effect in kainic acid (KA)-induced seizures. Here, we investigated the protective effects of atorvastatin pretreatment on KA-induced neuroinflammation and hippocampal cell death. Mice were treated via intragastric administration of atorvastatin for 7 days, injected with KA, and then sacrificed after 24 h. We observed that atorvastatin pretreatment reduced KA-induced seizure activity, hippocampal cell death, and neuroinflammation. Atorvastatin pretreatment also inhibited KA-induced lipocalin-2 expression in the hippocampus and attenuated KA-induced hippocampal cyclooxygenase-2 expression and glial activation. Moreover, AKT phosphorylation in KA-treated hippocampus was inhibited by atorvastatin pretreatment. These findings suggest that atorvastatin pretreatment may protect hippocampal neurons during seizures by controlling lipocalin-2-associated neuroinflammation.
