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目的观察乌司他丁对脑出血大鼠神经功能损伤及血肿周围组织MMP-9表达的影响。方法雄性SD大鼠100只按随机数字表法分为四组:模型组(30只)和治疗组(30只)大鼠右侧脑尾状核内注射自体血法建立脑出血模型;假手术组(30只)注射等容量生理盐水;对照组(10只)不作处理。造模成功后,治疗组尾静脉注入乌司他丁10万U/kg,模型组相应注射等体积生理盐水。于术后12h、1d、3d、7d和14d采用改良神经功能缺损评分(mNSS)评估模型组和治疗组大鼠神经功能损伤程度,并分别处死6只大鼠,采用干湿重法检测大鼠脑组织含水量,RT-PCR和免疫组化检测大鼠血肿周围脑组织中MMP-9mRNA和蛋白表达水平。结果与假手术组比较,模型组大鼠mNSS评分升高,脑组织含水量增加,MMP-9 mRNA和蛋白表达升高,以第3天最为显著(P<0.05);与模型组比较,治疗组大鼠mNSS评分下降,脑组织含水量、MMP-9mRNA和蛋白表达均减少(P<0.05)。结论乌司他丁可明显减轻大鼠脑出血后脑水肿和神经功能障碍。其机制可能与乌司他丁抑制出血后脑组织中MMP-9表达有关。
Objective To observe the effects of ulinastatin on neurological damage and the expression of MMP-9 in perihematomal brain tissue after intracerebral hemorrhage in rats. Methods One hundred male Sprague-Dawley rats were randomly divided into four groups according to the random number table: The model group (30 rats) and the treatment group (30 rats) were injected intracerebral caudate nucleus autologous blood to establish the intracerebral hemorrhage model. Group (30 rats) injected with normal saline; control group (10) without treatment. After successful modeling, the treatment group received ulinastatin at the tail vein of 100,000 U / kg, and the model group was injected with equal volume of normal saline. The rats were sacrificed at 12h, 1d, 3d, 7d and 14d after operation to evaluate the neurological deficits in model group and treatment group by modified neurological deficit score (mNSS). Six rats were sacrificed and the rats were sacrificed by dry-wet method Brain water content, RT-PCR and immunohistochemistry were used to detect the expression of MMP-9mRNA and protein in the perihematomal brain tissue of rats. Results Compared with the sham operation group, the mNSS score increased, the brain water content increased, the expression of MMP-9 mRNA and protein increased in the model group (P <0.05), compared with the model group The rats’ mNSS scores decreased, the water content of brain tissue and the expression of MMP-9 mRNA and protein decreased (P <0.05). Conclusion Ulinastatin can significantly reduce brain edema and neurological dysfunction after intracerebral hemorrhage in rats. The mechanism may be related to the inhibition of ulinastatin on the expression of MMP-9 in brain tissue after hemorrhage.