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Neuroprotection of Lithium is Associated with Inhibition of Bax Expression and Caspase 8 Activation

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Author(s)
Gee-youn KwonSoo-kyung Kim
Keimyung Author(s)
Kim, Soo Kyung
Department
Dept. of Pharmacology (약리학)
Journal Title
Korean J of Physiology & Pharmacology
Issued Date
2001
Volume
5
Issue
5
Keyword
BaxCaspase 8LithiumNMDANeuronal apoptosis
Abstract
Neuroprotective properties of lithium were investigated by using in vivo NMDA excitotoxicity model. The appearance of TUNEL positive cells was prominent within 24 h of NMDA (70 mg/kg, i.p.) injection in the regions of the cortex, hippocampal formation, and thalamus of mouse cerebrum. NMDA treatment resulted in the extensive enhancement of Bax immunoreactivity in the cortical and hippocampal regions. NMDA also increased the immunoreactivity of caspase 8 in the similar regions of the mouse cerebrum. However, the increased immunoreactivity of Bax and caspase 8 were dramatically attenuated by chronic lithium pretreatment (lithium chloride, 300 mg/kg/d, i.p. for $7{\sim}10$ 수식 이미지 days). At the same time, lithium ion blocked the appearance of TUNEL positive cells, and the morphological assessment indicated an effective neuroprotection by lithium against NMDA excitotoxicity. Although the exact action mechanism of lithium is not straightforward at this time, we propose that the inhibition of Bax and caspase cascade is involved in the neuroprotective action of lithium.


Keywords:
Bax; Caspase 8; Lithium; NMDA; Neuronal apoptosis
Keimyung Author(s)(Kor)
김수경
Publisher
School of Medicine
Citation
Gee-youn Kwon and Soo-kyung Kim. (2001). Neuroprotection of Lithium is Associated with Inhibition of Bax Expression and Caspase 8 Activation. Korean J of Physiology & Pharmacology, 5(5), 389–396.
Type
Article
ISSN
1226-4512
URI
https://kumel.medlib.dsmc.or.kr/handle/2015.oak/34622
Appears in Collections:
1. School of Medicine (의과대학) > Dept. of Pharmacology (약리학)
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