Nitric oxide produced during ischemia is toxic but crucial to preconditioning-induced ischemic tolerance of neurons in culture

被引：25

作者：

Kawahara, K ^{[1
]}

Yanoma, J ^{[1
]}

Tanaka, M ^{[1
]}

Nakajima, T ^{[1
]}

Kosugi, T ^{[1
]}

机构：

[1] Hokkaido Univ, Lab Biomed Control, Res Inst Elect Sci, Sapporo, Hokkaido 0600812, Japan

来源：

NEUROCHEMICAL RESEARCH | 2004年 / 29卷 / 04期

关键词：

ischemia; preconditioning; nitric oxide; neurotoxicity; cortical culture;

D O I：

10.1023/B:NERE.0000018853.30131.4d

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

The present study investigated the roles of nitric oxide ( NO) in preconditioning (PC)-induced neuronal ischemic tolerance in cortical cultures. Ischemia in vitro was simulated by subjecting cultures to both oxygen and glucose deprivation (OGD). A sublethal OGD (PC) significantly increased the survival rate of neurons when cultures were exposed to a lethal OGD 24 h later. Both the inhibition of nitric oxide synthase ( NOS) and scavenging of NO during PC significantly attenuated the PC-induced neuronal tolerance. In addition, exposure to an NO donor emulated the PC. In contrast, the inhibition of NOS and the scavenging of NO during lethal OGD tended to increase the survival rate of neurons. This study suggested that NO produced during ischemia was fundamentally toxic, but critical to the development of PC-induced neuronal tolerance.

引用

页码：797 / 804

页数：8

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