In mixed glial cell cultures from cerebral cortices of newborn rats, endotoxin induces inducible nitric oxide (iNOS), nitric oxide (NO), and interleukin-1 beta (IL-1 beta) production in microglial cells. Earlier we demonstrated that endotoxin induced iNOS but not IL-1 beta expression in microglial c
THERAPEUTIC STRATEGIES FOR THE INHIBITION OF INDUCIBLE NITRIC OXIDE SYNTHASE—POTENTIAL FOR A NOVEL CLASS OF ANTI-INFLAMMATORY AGENTS
✍ Scribed by JOSEF PFEILSCHIFTER; WOLFGANG EBERHARDT; RICHARD HUMMEL; DIETER KUNZ; HEIKO MÜHL; DOROTHEA NITSCH; CHRISTOPH PLÜSS; GABY WALKER
- Publisher
- Elsevier Science
- Year
- 1996
- Tongue
- English
- Weight
- 215 KB
- Volume
- 20
- Category
- Article
- ISSN
- 1065-6995
No coin nor oath required. For personal study only.
✦ Synopsis
In recent years, NO, a gas previously considered a potentially toxic chemical, has become established as a diffusible universal messenger mediating cell-cell communication throughout the body. In mammals, NO is a recognized mediator of blood vessel relaxation that helps to maintain blood pressure. In the central nervous system NO acts as a non-conventional neurotransmitter and participates in the establishment of long-term plasticity required for memory formation. In addition, NO is responsible for some parts of the host response to sepsis and inflammation and contributes to certain disease states. A number of strategies have emerged with regard to a pharmacological control of pathological NO overproductions. This review will discuss these novel therapeutic approaches that may provide new means for clinical medicine.
📜 SIMILAR VOLUMES