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Dexamethasone and nitric oxide synthase gene expression in brain
E Suzuki1, F Shintani, T Nakaki
1Department of Neuropsychiatry, Keio University School of Medicine, Tokyo, Japan.
Journal of Psychiatry & Neuroscience : JPN
|March 1, 1997
Summary
Systemic inflammation induced by lipopolysaccharide (LPS) activates type II inducible nitric oxide synthase (iNOS) gene expression in the rat brain. Dexamethasone (DEX) effectively suppresses this iNOS mRNA induction, suggesting a protective mechanism.
Area of Science:
- Neuroscience
- Immunology
- Pharmacology
Background:
- Systemic inflammation, triggered by lipopolysaccharide (LPS), is known to induce type II inducible nitric oxide synthase (iNOS) in peripheral tissues.
- The impact of systemic inflammation on iNOS expression within the brain remains an area requiring further investigation.
Purpose of the Study:
- To investigate whether intraperitoneal LPS administration induces iNOS mRNA expression in the rat brain.
- To determine if dexamethasone (DEX) treatment can prevent LPS-induced iNOS mRNA expression in the brain.
Main Methods:
- Quantitative reverse transcription-polymerase chain reaction (RT-PCR) was utilized to measure iNOS mRNA levels.
- Rats were administered LPS intraperitoneally to induce systemic inflammation.
- Dexamethasone (DEX) was administered intraperitoneally to assess its preventative effects.
Main Results:
- LPS administration led to a significant induction of iNOS mRNA in multiple brain regions.
- Induced iNOS mRNA levels ranged from approximately 1 x 10(5) to 4 x 10(5) molecules per microgram of poly A+ RNA.
- Concurrent treatment with DEX markedly suppressed the LPS-induced iNOS mRNA expression.
Conclusions:
- Systemic inflammation, induced by LPS, triggers iNOS mRNA expression in the rat brain.
- Dexamethasone exerts a suppressive effect on LPS-induced iNOS mRNA in the brain, indicating a DEX-sensitive regulatory mechanism.