抑肽酶对全氟异丁烯诱导大鼠急性肺损伤的影响及其机制

发布时间：2018-05-06 23:43

本文选题：抑肽酶 + 全氟异丁烯　；参考：《安徽医科大学学报》2014年11期

【摘要】：目的探讨蛋白酶抑制剂抑肽酶对全氟异丁烯(PFIB)诱导大鼠急性肺损伤(ALI)的影响及其机制。方法PFIB诱导建立大鼠ALI动物模型。将成年雄性SD大鼠40只按体重排序,以体重为区组因素随机分成5组:对照组(N组)、ALI组(I组)、5 mg/kg抑肽酶组(L组)、15 mg/kg抑肽酶组(M组)、30 mg/kg抑肽酶组(H组)。PFIB吸入30min后,I组经腹腔注射生理盐水,抑肽酶治疗组则经腹腔注射不同剂量(5、15、30 mg/kg)的抑肽酶溶液。24 h后收集各组支气管肺泡灌洗液(BALF)和血液,并测定各组的动脉血气值及肺湿/干质量比值,用BCA法测定支气管BALF总蛋白含量,ELISA法测定血清肿瘤坏死因子-α(TNF-α)和白介素-6(IL-6)的量,并在光镜下进行肺组织病理检查。结果 I组肺湿干重比、BALF总蛋白含量、IL-6、TNF-α水平较N组均明显升高(P0.05)。经抑肽酶治疗后,L组湿干重比、总蛋白含量水平与I组比较,差异无统计学意义(P0.05),IL-6、TNF-α水平有明显降低(P0.05)。H组湿干重比、总蛋白含量、IL-6、TNF-α水平均明显低于I组(P0.05),与L组、M组比较也有明显降低(P0.05)。染毒后大鼠pH值及氧分压明显下降,二氧化碳分压升高,经抑肽酶治疗后,pH值及氧分压有所提高,二氧化碳分压有所下降,以高剂量时改变最明显。肺组织病理组织学结果显示,抑肽酶能明显改善肺组织病理损伤,以高剂量最有效。结论抑肽酶能通过抑制细胞因子和炎症介质的释放来减轻大鼠ALI的肺部炎症反应。
[Abstract]:Objective to investigate the effect and mechanism of protease inhibitor aprotinin on acute lung injury induced by PFIBs in rats. Methods PFIB induced rat ALI model was established. Forty adult male Sprague-Dawley rats were ranked according to their body weight. Body weight was randomly divided into five groups: control group (n group) and control group (group I) with 5 mg/kg aprotinin group (group L) and group M with 15 mg/kg aprotinin group. The rats in group B were given intraperitoneal injection of normal saline after 30min inhalation in group H and mg/kg aprotinin group (P < 0.05), and the control group was given intraperitoneal injection of normal saline after 30min inhalation. In the aprotinin treatment group, the bronchoalveolar lavage fluid (BALFF) and blood were collected after intraperitoneal injection of aprotinin solution of different doses (515g / kg) for 24 h, and arterial blood gas and lung wet / dry weight ratio were measured. The total protein content of bronchial BALF was determined by BCA method. The serum levels of TNF- 伪 and IL-6 were determined by Elisa, and the lung histopathology was examined under light microscope. Results the content of BALF total protein and the level of IL-6 TNF- 伪 in group I were significantly higher than those in group N (P 0.05). After treatment with aprotinin, the wet / dry weight ratio and total protein content in group L were not significantly different from those in group I, and the level of IL-6 TNF- 伪 in group I was significantly lower than that in group I, and the ratio of wet dry weight to dry weight of group H was significantly lower than that of group I. The level of TNF- 伪 in group I was significantly lower than that in group I (P 0.05), and the level of TNF- 伪 in group M was significantly lower than that in group L (P 0.05). After treatment with aprotinin, the pH and partial pressure of oxygen decreased significantly, and the partial pressure of carbon dioxide increased. After aprotinin treatment, the pH and partial pressure of oxygen increased, and the partial pressure of carbon dioxide decreased. The histopathological results of lung tissue showed that aprotinin could significantly improve the pathological injury of lung tissue, and high dose was the most effective. Conclusion Aprotinin can inhibit the release of cytokines and inflammatory mediators to attenuate the pulmonary inflammation of ALI in rats.
【作者单位】：安徽医科大学解放军杭州临床学院(杭州128医院)心肺康复科;北京军事医学科学院毒物与药物研究所;
【基金】：2012南京军区重点课题基金(编号:11Z037)
【分类号】：R563.8

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