Brain iNOS: current understanding and clinical implications

被引：110

作者：

Licinio, J

Prolo, P

McCann, SM

Wong, ML

机构：

[1] NIMH, Clin Neuroendocrinol Branch, NIH, Bethesda, MD 20892 USA

[2] Louisiana State Univ, Pennington Biomed Res Ctr, Baton Rouge, LA 70808 USA

来源：

MOLECULAR MEDICINE TODAY | 1999年 / 5卷 / 05期

关键词：

D O I：

10.1016/S1357-4310(99)01453-7

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：

Nitric oxide (NO) is a unique informational substance first identified as the endothelium-derived relaxing factor. It is generated by NO synthases and plays a prominent role in controlling a variety of organ functions in the cardiovascular, immune, reproductive and nervous systems. Inducible nitric oxide synthase (iNOS) is not normally present in the brain in youth but it can be detected in the brain after inflammatory, infectious or ischemic damage, as well as in the normal, aging brain. Brain INOS seems to contribute to the pathophysiology of many diseases that involve the central nervous system, but the role of iNOS appears to go beyond tissue damage. Brain iNOS might be required for adequate repair following injury or damage. The effects of brain iNOS on the balance between damage and repair make this enzyme a promising therapeutic target in human disease.

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收藏

页码：225 / 232

页数：8

相关论文

共 59 条

[41] Neuronal expression of inducible nitric oxide synthase after oxygen and glucose deprivation in rat forebrain slices [J].

Moro, MA ;

De Alba, J ;

Leza, JC ;

Lorenzo, P ;

Fernández, AP ;

Bentura, ML ;

Boscá, L ;

Rodrigo, J ;

Lizasoain, I .

EUROPEAN JOURNAL OF NEUROSCIENCE, 1998, 10 (02) :445-456

[42]

Murad F, 1998, RECENT PROG HORM RES, V53, P43

[43] Delayed treatment with aminoguanidine decreases focal cerebral ischemic damage and enhances neurologic recovery in rats [J].

Nagayama, M ;

Zhang, FY ;

Iadecola, C .

JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 1998, 18 (10) :1107-1113

[44] NITRIC-OXIDE SYNTHASES - ROLES, TOLLS, AND CONTROLS [J].

NATHAN, C ;

XIE, QW .

CELL, 1994, 78 (06) :915-918

[45] AIDS dementia is associated with massive, activated HIV-1 infection and concomitant expression of several cytokines [J].

Nuovo, GJ ;

Alfieri, ML .

MOLECULAR MEDICINE, 1996, 2 (03) :358-366

[46] Nitric oxide via an inducible isoform of nitric oxide synthase is a possible factor to eliminate inflammatory cells from the central nervous system of mice with experimental allergic encephalomyelitis [J].

Okuda, Y ;

Sakoda, S ;

Fujimura, H ;

Yanagihara, T .

JOURNAL OF NEUROIMMUNOLOGY, 1997, 73 (1-2) :107-116

[47] EXPRESSION OF THE INDUCIBLE ISOFORM OF NITRIC-OXIDE SYNTHASE IN THE CENTRAL-NERVOUS-SYSTEM OF MICE CORRELATES WITH THE SEVERITY OF ACTIVELY INDUCED EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS [J].

OKUDA, Y ;

NAKATSUJI, Y ;

FUJIMURA, H ;

ESUMI, H ;

OGURA, T ;

YANAGIHARA, T ;

SAKODA, S .

JOURNAL OF NEUROIMMUNOLOGY, 1995, 62 (01) :103-112

[48] Inducible nitric oxide synthase in Theiler's murine encephalomyelitis virus infection [J].

Oleszak, EL ;

Katsetos, CD ;

Kuzmak, J ;

Varadhachary, A .

JOURNAL OF VIROLOGY, 1997, 71 (04) :3228-3235

[49] EVIDENCE FOR A ROLE OF NITRIC-OXIDE IN THE CORTICOTROPIN-RELEASING FACTOR RELEASE INDUCED BY INTERLEUKIN-1-BETA [J].

SANDI, C ;

GUAZA, C .

EUROPEAN JOURNAL OF PHARMACOLOGY, 1995, 274 (1-3) :17-23

[50] Microglial NO induces delayed neuronal death following acute injury in the striatum [J].

Takeuchi, A ;

Isobe, K ;

Miyaishi, O ;

Sawada, M ;

Fan, ZH ;

Nakashima, I ;

Kiuchi, K .

EUROPEAN JOURNAL OF NEUROSCIENCE, 1998, 10 (05) :1613-1620

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