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Effect of Urinary Kallidinogenase on Transforming Growth Factor-β1 and High-Sensitivity C-Reactive Protein Expression in Rat Focal Cerebral Ischemic Injury

机译:尿环磷酰胺原酶对大鼠局灶性脑缺血损伤中转化生长因子-β1和高敏C反应蛋白表达的影响

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BACKGROUND In this study we investigated the effect of urinary kallidinogenase (UK) on transforming growth factor beta 1 (TGF-β1) expression in brain tissue. We also explored the neuroprotective mechanism of UK against ischemic injury by measuring serum high-sensitivity C-reactive protein (hs-CRP) level changes after rat cerebral ischemic injury. MATERIAL AND METHODS The rat middle cerebral artery ischemia/reperfusion model was established using the suture method. Sprague-Dawley rats were randomly divided into 3 groups: treatment, [i]Gegen[/i] control, and blank control. Each group was subsequently divided into 5 subgroups according to time (6, 12, 24, 48, and 72 h). Rats in the treatment group were administered UK as treatment. TGF-β1 expression was observed at each time point using SABC and immunohistochemical staining methods to estimate cerebral infarct volume percentage. Serum hs-CRP levels were also measured. RESULTS TGF-β1 protein expression in ischemic brain tissues of the treatment group significantly increased at each time point ([i]P[/i]<0.01) compared with both control groups. Treatment group serum hs-CRP levels significantly decreased at each time point (P<0.05) compared with both control groups. CONCLUSIONS UK exerts a neuroprotective effect by upregulating TGF-β1 expression and inhibiting excessive inflammatory responses.
机译:背景技术在这项研究中,我们调查了尿中的尿苷激肽原酶(UK)对脑组织中转化生长因子β1(TGF-β1)表达的影响。我们还通过测量大鼠脑缺血损伤后血清高敏C反应蛋白(hs-CRP)水平的变化,探索了UK抗缺血损伤的神经保护机制。材料与方法采用缝合法建立大鼠大脑中动脉缺血/再灌注模型。将Sprague-Dawley大鼠随机分为3组:治疗,Gegen对照和空白对照组。随后根据时间(6、12、24、48和72小时)将每个组分为5个子组。治疗组中的大鼠接受UK治疗。使用SABC和免疫组织化学染色方法在每个时间点观察TGF-β1表达,以估计脑梗死体积百分比。还测量了血清hs-CRP水平。结果与两个对照组相比,治疗组缺血性脑组织中TGF-β1蛋白的表达在每个时间点均显着增加([i] P [/ i] <0.01)。与两个对照组相比,治疗组在每个时间点的血清hs-CRP水平均显着降低(P <0.05)。结论UK通过上调TGF-β1的表达并抑制过度的炎症反应发挥神经保护作用。

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