| Objectives: To study the effect of neuregulin-1? on the expression of superoxide dismutase and quinone oxidoreductase in intracerebral hemorrhage and Evaluate the brain edema and neurological dysfunction.To explore the neuroprotective effect and mechanism of NRG-1? in ICH.Methods: A healthy male Sprague–Dawley rats were used to establish a rat model of intracerebral hemorrhage by injecting collagenase into the caudate nucleus.Sham operation group of 12 male SD rats were injected with saline at the same position.48 successful ICH model rats were included in the statistical range and randomly divided into model group and NRG-1? treatment group(2ug/kg)with each group of 24 rats.Each group was divided into 24 h and 72 h two time points.Each time point was subdivided into two subgroups.In sham operation group,every time points have 6 rats.There are 12 rats at each time point in Model group and NRG-1? treatment group.The rats were sacrificed at the time point.Using the modified neurological severity score(m NSS)were assessed in rat neural dysfunction,The expression levels of SOD and NQO1 with surrounding tissue after intracerebral hemorrhage in rats were detected by Western blot analysis and immunohistochemistry,and the brain water content were evaluated by dry wet weight method.Results:1.Compared with the sham operation group,the water content in the brain tissue of the model group and the NRG-1? treatment group increased significantly in the time points of 24 h and 72 h after ICH and there was statistical significance(P<0.05);Compared with the model group,the water content of the brain tissue in the NRG-1?treatment group decreased at each time point,and the statistical analysis was significant(P<0.05),suggesting that NRG-1? can relieve the degree of cerebral edema in the acute stage of ICH.2.Compared with sham operation group,model group and NRG-1? treatment group nerve dysfunction in rats after ICH 24 h and 72 h time points,there was statisticalsignificance(P<0.05);Compared with the model group at the same time,NRG-1?treatment group nerve dysfunction was significantly reduced,statistically meaningful(P<0.05).These results suggest that NRG-1? can improve neurological deficits in ICH acute phase.3.The results of immunohistochemistry showed that only scattered SOD and NQO1 positive granule cells could be seen in the sham operated group,but there was no significant difference in each time point;At the 24 h and 72 h time points,the model group and the NRG-1? treatment group could observe the obvious expression of SOD and NQO1 positive granules in the surrounding tissues of ICH rats,and the neurons,microglia and neutrophils were common;Compared with the model group,the number of SOD and NQO1 positive particles in the NRG-1? treatment group was more significant at the same time point,the difference was statistically significant(P<0.05).These results indicate that NRG-1? can up regulate the expression of antioxidant enzymes SOD and NQO1 in the acute phase of ICH.4.Immunohistochemical staining showed that the SOD and NQO1 protein bands in the model group and the NRG-1? group could be seen in the 24 h and 72 h time points after ICH in each group of rats;Compared with the sham operation group,the relative protein gray values of SOD and NQO1 were higher in the model group and the NRG-1?treatment group at each time point(P<0.05),the difference was statistically significant;The SOD and NQO1 relative protein gray levels of the NRG-1? treatment group were higher than that of the model group at each time point,and the statistical analysis was significant(P<0.05),indicating that NRG-1? can up regulate the levels of antioxidant enzymes SOD and NQO1 in the acute phase after ICH in rats.Conclusion: In the acute phase of ICH damage,NRG-1? can increase the levels of antioxidant enzymes SOD and NQO1,reduce free radical production,reduce oxidative stress,significantly improve cerebral edema and neurological dysfunction,and play a neuroprotective role. |
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