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The Impact of DETA-NONOate on NADPH Oxidase-derived Oxidative Stress in Rats after Stroke

Author: JiangZheng
Tutor: HuZhiPing
School: Central South University
Course: Neurology
Keywords: Ischemic stroke NO donor DETA-NONOate NADPH oxidase Oxidative Stress
CLC: R743.3
Type: Master's thesis
Year: 2011
Downloads: 35
Quote: 0
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Abstract


Objective: To detect NO donor DETA-NONOate middle cerebral artery occlusion / reperfusion (MCAO / reperfusion ) in rat brain tissue NADPH oxidase activity , DETA-NONOate treatment of ischemic stroke protection its mechanism . Methods: SD rats were randomly divided into sham-operated group , MCAO / reperfusion group and MCAO / reperfusion DETA-NONOate intervention group . Suture method in rat MCAO / reperfusion model after ischemia 1h unplug the line tied into the reperfusion period . 10-15min after reperfusion intervention group the intravenous injection of DETA-NONOate (0.4mg/kg). Part MCAO rats neurological deficit scores reperfusion period , 24 hours after the rats were killed and neck breaking method the TTC staining evaluation of cerebral infarct volume . The remaining rats after reperfusion 4 hours to extract the brain tissue , brain tissue was measured lipid peroxidation products MDA content , brain tissue NO levels and NADPH oxidase activity , Western blot determination of the NADPH oxidase subunits ( p22phox , p47phox Nox2/gp91phox, Nox and Rac-1) expression . Results : 1 ) DETA- NONOate to reduce 1hMCAO/24h reperfusion rat cerebral infarction volume ( P lt; 0.01 ) improve stroke in rats after 12h , 24h neurological deficit symptoms ( P lt; 0.05 ) ; 2 ) large mouse 1hMCAO/4h reperfusion brain tissue lipid peroxidation product MDA levels higher than the sham group (P lt; 0.05), DETA-NONOate intervention in brain tissue MDA levels decreased compared with the control group ( P lt; 0.05 ) ; 3) 1hMCAO rats in reperfusion initial intravenous use of DETA-NONOate can improve reperfusion 4h brain tissue NO levels (P lt; 0.05); 4) DETA-NONOate reduce 1hMCAO/4h reperfusion in rat brain tissue NADPH oxidase activity of (P lt; 0.01); 5) DETA-NONOate 1hMCAO/4h reperfusion in rat brain tissue NADPH oxidase subunit p22phox , p47phox and Rac-1 expression was decreased ( P lt; 0.05 ) . Conclusion: NO donor DETA-NONOate can improve the neurological deficit symptoms of ischemic stroke in rats , inhibition of NADPH oxidase activity and expression in rat brain tissue against ischemic stroke oxidative stress , thus missing brain tissue blood and secondary reperfusion injury to play a neuroprotective effect .

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CLC: > Medicine, health > Neurology and psychiatry > Neurology > Cerebrovascular disease > Acute cerebrovascular disease ( stroke)
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