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Changes of MDA、NF-κB、TNF-α in Brain Tissue and Plasma Following Intracerebral Hemorrhage in Rats and the Intervention of Edaravone

Author: CuiJie
Tutor: WangJingZhou
School: Third Military Medical University
Course: Neurology
Keywords: Cerebral hemorrhage Brain water content Malondialdehyde Nuclear factor-κB Tumor necrosis factor -α Edaravone
CLC: R743.34
Type: Master's thesis
Year: 2007
Downloads: 215
Quote: 1
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Abstract

Background and Purpose cerebral hemorrhage (intracerebral hemorrhage, ICH) is the primary brain parenchymal hemorrhage, with a high incidence and high mortality, morbidity, serious threat to human life and health. Intracerebral hemorrhage surrounding tissue edema and neuronal damage is an important factor to affect the severity and prognosis of patients with cerebral hemorrhage. Cerebral hemorrhage However there is no precise and effective treatment method. The main reason is not entirely clear understanding of its pathophysiological mechanisms. The study found intracerebral hemorrhage around the \process. Further studies after cerebral hemorrhage perihematoma pathophysiological mechanisms and intervention, is important to reduce the patient's functional damage, and improve clinical outcomes. Radical and its related inflammatory mechanisms such damages are more and more attention. Radical scavenger MCI-186 (3 - methyl-1 - phenyl-2 - pyrazolin-5 - one, according edaravone) as the development of a new anti-oxidants have been widely used for the treatment of acute cerebral infarction. a significant effect. Hemorrhagic brain injury have a therapeutic effect is unclear. This study by observing radical and inflammatory reaction hemorrhage brain injury, and edaravone on cerebral hemorrhage whether or not to have a therapeutic effect and to explore its possible mechanism, pathophysiological mechanisms for hemorrhage brain injury research and clinical The treatment provides a theoretical basis. Materials and Methods Animal groups: 120 Sprague-Dawley Rats, male and female, according to the random number table is divided into a control group (Control group), patients with cerebral hemorrhage (ICH group) and treatment group (Therapy group) , 40 in each group. Each different time points are divided into four sub-groups, each sub-group of 10. 5 for brain water content and pathology detection, and another five for MDA, TNF-α, NF-κB is detected. Rats in each group before the brain was removed, blood samples were collected from the inferior vena cava, detection indicators plasma. ICH animal models: Stereotactic autologous blood injection method. Along the midline incision of the skin of the head exposed skull, and Bregma Point (anterior fontanelle). The open the 3mm at vertical needle into 6mm in the anterior fontanelle front 0.2mm, next to the center line of the right side to reach the caudate nucleus, twice injected 50ul autologous blood. 3 the control rats steps with ICH group, but does not inject blood. Treated rats at modeling 30min before and modeling 1 / 12h is injected intraperitoneally of edaravone (3mg/Kg); ICH group and the control group rats were injected with saline. 4 neurological deficit scores: reference Longa (1989) standards. Brain water content detection: wet and dry weight. Formula: brain water content = (wet weight - dry weight) / wet weight × 100%. 6. MDA detection: thiobarbituric acid method the unit: nmol / mgprot,. 7. TNF-α detection: enzyme-linked immunosorbent assay (ELISA) method, unit: ng / ml. 8. NF-κB detection: electrophoretic mobility shift assay (EMSA) method, Unit: DU. 9. Pathology analysis: hematoxylin - eosin (HE), observed under light microscope. 10 Statistical analysis: application SPSS10.0 statistical software for univariate analysis of variance and related inspection. Results neurological deficit Rating: cerebral hemorrhage rats at each time phase point neurological deficit score was significantly higher than that in the control group; treated rats at each time point neurological deficit scores were significantly lower than the cerebral hemorrhage group (P lt; 0.05). Brain water content detection: cerebral hemorrhage rats 6h, 24h, 72h brain water content compared with the control group was significantly higher (P lt; 0.05), the 168h was no significant difference (P gt; 0.05); compared with cerebral hemorrhage group treatment of rats 6h, 24h, 72h brain water content was significantly lower (P lt; 0.05), 168h difference was not significant (P gt; 0.05). Brain homogenate MDA, TNF-α content detection: ICH group rats at all time points brain homogenate MDA, TNF-α content was significantly higher than the control group (P lt; 0.05); compared with the patients with cerebral hemorrhage treated rats brain homogenates MDA, TNF-α levels were significantly lower (P lt; 0.05). Correlation test results: cerebral hemorrhage group and the treatment group rat brain water content and brain homogenates of TNF-α content was a significant positive correlation, the correlation coefficient R2 = 0.934, p lt; 0.01 5 NF-κB activity of brain tissue detection: cerebral hemorrhage group compared with the control group, rats in each time relative to the point of brain tissue NF-κB activity very significantly higher (p lt; 0.01); compared with cerebral hemorrhage group, the treatment group rat brain tissue at all time points, NF-κB The activity is very significantly lower (p lt; 0.01). 6 plasma MDA, TNF-α content detection: cerebral hemorrhage group at all time points plasma MDA, TNF-α content compared with the control group was significantly higher (p lt; 0.01); compared with cerebral hemorrhage group treated rats plasma MDA, TNF-α content very significantly reduce (P lt; 0.01). Pathological changes of brain tissue: HE staining under light microscope to see infiltration of inflammatory cells and edema around the hematoma cerebral hemorrhage rats than in the control group were serious; treated rats with cerebral hemorrhage group compared eased significantly. Conclusion 1. Radicals after cerebral hemorrhage a lot of produce, the excessive release of TNF-α and hematoma surrounding tissue edema, is closely related to the pathophysiological mechanism of neuronal damage. 2 after cerebral hemorrhage free radical generation, and may further result in NF-κB activation, the excessive release of TNF-α in its downstream. Confirmed that rats with intracerebral hemorrhage related to massive release of inflammatory mechanisms and radical. 3. Edaravone exact role in the protection of nerve tissue in the brain hemorrhage. Its mechanism may be associated with free radical scavenging against lipid peroxidation, as well as indirectly inhibit the inflammatory response.

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