2003•Chinese Journal of Neuroimmunology and NeurologyRequires access

The Relationship between the Gene Expression of Inducible Nitric Oxide Synthase and Brain Cells Apoptosis following Cerebral Hypoxia-ischemia

Shu Pu

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Abstract

Objective To investigate the relationship between the gene expression of theinduciblenitric oxidesynthase(iNOS)andbraincellsapoptosisfollowing cerebral hypoxia ischemia in the neonatal rats.Methods 7 day old rat pups were subjected to a unilateral ligation of the common carotid artery followed by a 2 h 30 min stay in the prearranged hypoxic chamber (8%O 2 in N 2). Rapid competitive reverse transcriptase PCR and in situ end labeling methods were used to detect the expression of iNOS mRNA and brain cells apoptosis separately in the hemisphere subjected to both ligation and hypoxia suffered at different time points from hypoxia ischemia.Results In the ipsilateral hemisphere following cerebral hypoxia ischemia, the expression ofiNOSmRNA began at 6 h(0.41±0 13), peaked at 24 h(2 02±0 24), and returned to baseline at 7 days. The evident increase of apoptotic cells in the ipsilateral hemisphere began at 6 h following hypoxia ischemia[(21 3±3 5)/10 hpf], peaked at 24 h[(63 7±3 2)/10 hpf], which was higher than that of the control[(7 3±2 3)/10 hpf, P0 01]. The peak time of the overexpression of iNOS mRNA was coordinated with that of apoptosis following hypoxia ischemia.Conclusions The increase in expression of iNOS mRNA and the brain cell apoptosis could be induced by cerebral hypoxia ischemia in neonatal rats.The overexpression of iNOS might play a role in the induction of apoptosis following cerebral hypoxia ischemia.

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Objective To investigate the relationship between the gene expression of theinduciblenitric oxidesynthase(iNOS)andbraincellsapoptosisfollowing cerebral hypoxia ischemia in the neonatal rats.Methods 7 day old rat pups were subjected to a unilateral ligation of the common carotid artery followed by a 2 h 30 min stay in the prearranged hypoxic chamber (8%O 2 in N 2). Rapid competitive reverse transcriptase PCR and in situ end labeling methods were used to detect the expression of iNOS mRNA and brain cells apoptosis separately in the hemisphere subjected to both ligation and hypoxia suffered at different time points from hypoxia ischemia.Results In the ipsilateral hemisphere following cerebral hypoxia ischemia, the expression ofiNOSmRNA began at 6 h(0.41±0 13), peaked at 24 h(2 02±0 24), and returned to baseline at 7 days. The evident increase of apoptotic cells in the ipsilateral hemisphere began at 6 h following hypoxia ischemia[(21 3±3 5)/10 hpf], peaked at 24 h[(63 7±3 2)/10 hpf], which was higher than that of the control[(7 3±2 3)/10 hpf, P0 01]. The peak time of the overexpression of iNOS mRNA was coordinated with that of apoptosis following hypoxia ischemia.Conclusions The increase in expression of iNOS mRNA and the brain cell apoptosis could be induced by cerebral hypoxia ischemia in neonatal rats.The overexpression of iNOS might play a role in the induction of apoptosis following cerebral hypoxia ischemia.

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Available abstract

Objective To investigate the relationship between the gene expression of theinduciblenitric oxidesynthase(iNOS)andbraincellsapoptosisfollowing cerebral hypoxia ischemia in the neonatal rats.Methods 7 day old rat pups were subjected to a unilateral ligation of the common carotid artery followed by a 2 h 30 min stay in the prearranged hypoxic chamber (8%O 2 in N 2). Rapid competitive reverse transcriptase PCR and in situ end labeling methods were used to detect the expression of iNOS mRNA and brain cells apoptosis separately in the hemisphere subjected to both ligation and hypoxia suffered at different time points from hypoxia ischemia.Results In the ipsilateral hemisphere following cerebral hypoxia ischemia, the expression ofiNOSmRNA began at 6 h(0.41±0 13), peaked at 24 h(2 02±0 24), and returned to baseline at 7 days. The evident increase of apoptotic cells in the ipsilateral hemisphere began at 6 h following hypoxia ischemia[(21 3±3 5)/10 hpf], peaked at 24 h[(63 7±3 2)/10 hpf], which was higher than that of the control[(7 3±2 3)/10 hpf, P0 01]. The peak time of the overexpression of iNOS mRNA was coordinated with that of apoptosis following hypoxia ischemia.Conclusions The increase in expression of iNOS mRNA and the brain cell apoptosis could be induced by cerebral hypoxia ischemia in neonatal rats.The overexpression of iNOS might play a role in the induction of apoptosis following cerebral hypoxia ischemia.

Key concepts: Hypoxia (environmental), Ischemia, Apoptosis, Nitric oxide synthase, Ligation, Nitric oxide, Messenger RNA, Endocrinology

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