脂氧素受体激动剂BML-111减轻大鼠机械通气肺损伤

发布时间：2018-07-09 17:51

本文选题：机械通气肺损伤 + 脂氧素　；参考：《临床麻醉学杂志》2014年03期

【摘要】：目的探讨脂氧素受体激动剂BML-111对机械通气肺损伤(VILI)的保护作用及其机制。方法 32只健康雄性SD大鼠随机均分四组,L组:VT6ml/kg;H组:VT20ml/kg;BML组:VT20ml/kg,机械通气开始时腹腔注射BML-111(1mg/kg);BOC组:VT20ml/kg,机械通气开始前30min腹腔注射叔丁氧羟基-苯丙氨酸-亮氨酸-苯丙氨酸-亮氨酸-苯丙氨酸(BOC-2,50μg/kg),机械通气开始时腹腔注射BML-111(1mg/kg)。RR均为80次/分,机械通气时间均为4h。实验结束处死大鼠,收集支气管肺泡灌洗液(BALF)和肺组织标本。观察肺组织病理学变化,Western Blot法检测肺组织中丝裂原活化蛋白激酶(MAPK)磷酸化水平、核转录因子(NF)-κB核转位。对BALF中细胞进行分类计数,检测BALF中炎症因子TNF-α、IL-1β、IL-6表达水平。结果 H、BOC组BALF中蛋白浓度和中性粒细胞计数、TNF-α、IL-1β和L-6含量明显高于L和BML组(P0.05或P0.01)。H、BOC组ERK、p38MAPK和JNK磷酸化水平明显高于L和BML组(P0.05或P0.01)。H、BOC组IKB-α表达明显低于L和BML组(P0.05或P0.01);H、BOC组NF-κB p65亚基从胞浆向胞核转位明显高于L和BML组(P0.05或P0.01)。结论 BML-111抑制MAPK的磷酸化和NF-κB信号通路激活,并可能是其减轻VILI的机制之一。
[Abstract]:Objective to investigate the protective effect of lipoxygen-receptor agonist BML-111 on mechanical ventilation lung injury (Vili) and its mechanism. Methods Thirty-two healthy male Sprague-Dawley rats were randomly divided into four groups: group L: VT6ml / kgH group: VT20ml / kg BML group. At the beginning of mechanical ventilation, BML-111 (1mg/kg) and BOC group (BOC group) were injected intraperitoneally with tert-butoxy-phenylalanine (30min) -leucine-phenylalanine (30min) at the beginning of mechanical ventilation. Leucine-phenylalanine (BOC-2N) 50 渭 g/kg, BML-111 (1mg/kg). RR were 80 times per minute at the beginning of mechanical ventilation. The mechanical ventilation time was 4 h. At the end of the experiment, the bronchoalveolar lavage fluid (BALF) and lung tissue were collected. The expression of mitogen activated protein kinase (MAPK) phosphorylation and nuclear translocation of nuclear transcription factor (NF)-魏 B were detected by Western blot. BALF cells were classified and counted to detect the expression of TNF- 伪 and IL-1 尾-尾 and IL-6 in BALF. Results the protein concentration and neutrophil count in BALF of HnBOC group were significantly higher than those of L and BML group (P0.05 or P0.01). The phosphorylation level of ERKp38MAPK and JNK in HnBOC group was significantly higher than that in L and BML group (P0.05 or P0.01). The expression of IKB- 伪 in HBOC group was significantly lower than that in L and BML group (P0.05 or P0.01). The translocation of NF- 魏 B p65 subunit from cytoplasm to nucleus was significantly higher in group N than in group L and BML (P0.05 or P0.01). Conclusion BML-111 inhibits the phosphorylation of MAPK and the activation of NF- 魏 B signaling pathway, which may be one of its mechanisms to reduce VILI.
【作者单位】：华中科技大学同济医学院附属协和医院ICU;
【基金】：国家自然基金重点项目(No.30930089) 卫生部临床重点学科项目(2010-47)
【分类号】：R563

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