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Effect of Dexamethasone on Inducible Nitric Oxide Synthase Gene Expression in Brain after Cerebral Hypoxia ischemia

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Abstract

Objective To investigate the gene expression of the inducible nitric oxide synthase(iNOS) in brain after cerebral hypoxia ischemia in neonatal rats and the effects of dexamethasone(DEX) on iNOS gene expression, so as to elucidate the possible mechanism of the neuroprotective effect of DEX administered to the rat pup prior to cerebral hypoxia ischemia. Methods Rapid competitive reverse transcriptase PCR was used to analyze semi quantitatively the expression of iNOS mRNA in brain at ipsilateral hemisphere in neonatal rats divided into five groups (1) hypoxia ischemia without DEX treatment;(2) hypoxia ischemia pre treatment with DEX;(3) hypoxia ischemia treated with DEX immediately,(4) sham pre treatment with DEX the normal controls. Results In the ipsilateral hemisphere following cerebral hypoxia ischemia, the expression of iNOS mRNA began at 6h, peaked at 24h, and returned to baseline at 7 days(n=3/time point). It was found that DEX administered to the neonatal rats prior to hypoxia ischemia could inhibit the expression of iNOS mRNA in the ipsilateral hemisphere, while DEX administered to the rats immediately following hypoxia ischemia seemed not to regulate the expression of iNOS mRNA probably. Conclusion NO production may play an important pathogenic role in the progression of the tissue damage that follows cerebral hypoxia ischemia. DEX exerts its neuroprotective effect partially through inhibiting the expression of iNOS mRNA.

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Objective To investigate the gene expression of the inducible nitric oxide synthase(iNOS) in brain after cerebral hypoxia ischemia in neonatal rats and the effects of dexamethasone(DEX) on iNOS gene expression, so as to elucidate the possible mechanism of the neuroprotective effect of DEX administered to the rat pup prior to cerebral hypoxia ischemia. Methods Rapid competitive reverse transcriptase PCR was used to analyze semi quantitatively the expression of iNOS mRNA in brain at ipsilateral hemisphere in neonatal rats divided into five groups (1) hypoxia ischemia without DEX treatment;(2) hypoxia ischemia pre treatment with DEX;(3) hypoxia ischemia treated with DEX immediately,(4) sham pre treatment with DEX the normal controls. Results In the ipsilateral hemisphere following cerebral hypoxia ischemia, the expression of iNOS mRNA began at 6h, peaked at 24h, and returned to baseline at 7 days(n=3/time point). It was found that DEX administered to the neonatal rats prior to hypoxia ischemia could inhibit the expression of iNOS mRNA in the ipsilateral hemisphere, while DEX administered to the rats immediately following hypoxia ischemia seemed not to regulate the expression of iNOS mRNA probably. Conclusion NO production may play an important pathogenic role in the progression of the tissue damage that follows cerebral hypoxia ischemia. DEX exerts its neuroprotective effect partially through inhibiting the expression of iNOS mRNA.

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Available abstract

Objective To investigate the gene expression of the inducible nitric oxide synthase(iNOS) in brain after cerebral hypoxia ischemia in neonatal rats and the effects of dexamethasone(DEX) on iNOS gene expression, so as to elucidate the possible mechanism of the neuroprotective effect of DEX administered to the rat pup prior to cerebral hypoxia ischemia. Methods Rapid competitive reverse transcriptase PCR was used to analyze semi quantitatively the expression of iNOS mRNA in brain at ipsilateral hemisphere in neonatal rats divided into five groups (1) hypoxia ischemia without DEX treatment;(2) hypoxia ischemia pre treatment with DEX;(3) hypoxia ischemia treated with DEX immediately,(4) sham pre treatment with DEX the normal controls. Results In the ipsilateral hemisphere following cerebral hypoxia ischemia, the expression of iNOS mRNA began at 6h, peaked at 24h, and returned to baseline at 7 days(n=3/time point). It was found that DEX administered to the neonatal rats prior to hypoxia ischemia could inhibit the expression of iNOS mRNA in the ipsilateral hemisphere, while DEX administered to the rats immediately following hypoxia ischemia seemed not to regulate the expression of iNOS mRNA probably. Conclusion NO production may play an important pathogenic role in the progression of the tissue damage that follows cerebral hypoxia ischemia. DEX exerts its neuroprotective effect partially through inhibiting the expression of iNOS mRNA.

Key concepts: Hypoxia (environmental), Nitric oxide synthase, Ischemia, Neuroprotection, Dexamethasone, Endocrinology, Nitric oxide, Internal medicine

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Effect of Dexamethasone on Inducible Nitric Oxide Synthase Gene Expression in Brain after Cerebral Hypoxia ischemia — Research Paper | ScholarLens