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

• 영문명: Neuroprotection of Lithium is Associated with Inhibition of Bax Expression and Caspase 8 Activation
• 발행기관: 대한생리학회-대한약리학회
• 저자명: Gee-youn Kwon Soo-kyung Kim
• 간행물 정보: 『The Korean Journal of Physiology & Pharmacology』제5권 제5호, 389~396쪽, 전체 8쪽
• 주제분류: 의약학 > 의학일반
• 파일형태: PDF
• 발행일자: 2001.01.01

영문 초록

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∼10 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.

키워드

Bax Caspase 8 Lithium NMDA Neuronal apoptosis