2006Journal of Jilin UniversityRequires access

Relationship between nitric oxide and superoxide dismutase in different brain tissues in delayed neuronal death rats

Jianying Zhang

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Abstract

Objective To study the influences of nitric oxide (NO) and superoxide dismutase (SOD) in genesis and progress of delayed neuronal death (DND) in rats. Methods Wistar rats were used to establish the models of four-vessel occlusion (4VO) and were treated with small dose of nitric oxide synthase (NOS) inhibitor [N-nitro-L-arginine (NNLA)]. The levels of NO and SOD in the brain tissues of the models were determined by spectrophotometry. Results The level of NO x (NO2 + NO3 ) in the experiment group was not significantly increased compared with control group (P0. 05). When reperfusion time was prolonged, the level of NO in the experiment group was decreased gradually and was lower than that in control group (P0. 05 or 0. 01). The level of SOD in hippocampus region was decreased distinctly (P0. 05 or 0. 01) and was not influenced by NNLA. The relativity analysis showed that the levels of NO and SOD in brain tissues were highly relative (r=0. 9624, P0. 05 or 0. 01). Conclusion Small dose of NOS inhibitor has the effect to protect neuron in DND rats. SOD can not only clean out superoxide negativeion, but also eliminate reactive oxygen species of NO x.

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Objective To study the influences of nitric oxide (NO) and superoxide dismutase (SOD) in genesis and progress of delayed neuronal death (DND) in rats. Methods Wistar rats were used to establish the models of four-vessel occlusion (4VO) and were treated with small dose of nitric oxide synthase (NOS) inhibitor [N-nitro-L-arginine (NNLA)]. The levels of NO and SOD in the brain tissues of the models were determined by spectrophotometry. Results The level of NO x (NO2 + NO3 ) in the experiment group was not significantly increased compared with control group (P0. 05). When reperfusion time was prolonged, the level of NO in the experiment group was decreased gradually and was lower than that in control group (P0. 05 or 0. 01). The level of SOD in hippocampus region was decreased distinctly (P0. 05 or 0. 01) and was not influenced by NNLA. The relativity analysis showed that the levels of NO and SOD in brain tissues were highly relative (r=0. 9624, P0. 05 or 0. 01). Conclusion Small dose of NOS inhibitor has the effect to protect neuron in DND rats. SOD can not only clean out superoxide negativeion, but also eliminate reactive oxygen species of NO x.

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Available abstract

Objective To study the influences of nitric oxide (NO) and superoxide dismutase (SOD) in genesis and progress of delayed neuronal death (DND) in rats. Methods Wistar rats were used to establish the models of four-vessel occlusion (4VO) and were treated with small dose of nitric oxide synthase (NOS) inhibitor [N-nitro-L-arginine (NNLA)]. The levels of NO and SOD in the brain tissues of the models were determined by spectrophotometry. Results The level of NO x (NO2 + NO3 ) in the experiment group was not significantly increased compared with control group (P0. 05). When reperfusion time was prolonged, the level of NO in the experiment group was decreased gradually and was lower than that in control group (P0. 05 or 0. 01). The level of SOD in hippocampus region was decreased distinctly (P0. 05 or 0. 01) and was not influenced by NNLA. The relativity analysis showed that the levels of NO and SOD in brain tissues were highly relative (r=0. 9624, P0. 05 or 0. 01). Conclusion Small dose of NOS inhibitor has the effect to protect neuron in DND rats. SOD can not only clean out superoxide negativeion, but also eliminate reactive oxygen species of NO x.

Key concepts: Superoxide dismutase, Nitric oxide, Nitric oxide synthase, Hippocampus, Chemistry, Neuronal Nitric Oxide Synthase, Reactive oxygen species, Internal medicine

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