本文選題：機械通氣肺損傷 + 脂氧素�。� 參考：《臨床麻醉學(xué)雜志》2014年03期

【摘要】：目的探討脂氧素受體激動劑BML-111對機械通氣肺損傷(VILI)的保護作用及其機制。方法 32只健康雄性SD大鼠隨機均分四組,L組:VT6ml/kg;H組:VT20ml/kg;BML組:VT20ml/kg,機械通氣開始時腹腔注射BML-111(1mg/kg);BOC組:VT20ml/kg,機械通氣開始前30min腹腔注射叔丁氧羥基-苯丙氨酸-亮氨酸-苯丙氨酸-亮氨酸-苯丙氨酸(BOC-2,50μg/kg),機械通氣開始時腹腔注射BML-111(1mg/kg)。RR均為80次/分,機械通氣時間均為4h。實驗結(jié)束處死大鼠,收集支氣管肺泡灌洗液(BALF)和肺組織標(biāo)本。觀察肺組織病理學(xué)變化,Western Blot法檢測肺組織中絲裂原活化蛋白激酶(MAPK)磷酸化水平、核轉(zhuǎn)錄因子(NF)-κB核轉(zhuǎn)位。對BALF中細胞進行分類計數(shù),檢測BALF中炎癥因子TNF-α、IL-1β、IL-6表達水平。結(jié)果 H、BOC組BALF中蛋白濃度和中性粒細胞計數(shù)、TNF-α、IL-1β和L-6含量明顯高于L和BML組(P0.05或P0.01)。H、BOC組ERK、p38MAPK和JNK磷酸化水平明顯高于L和BML組(P0.05或P0.01)。H、BOC組IKB-α表達明顯低于L和BML組(P0.05或P0.01);H、BOC組NF-κB p65亞基從胞漿向胞核轉(zhuǎn)位明顯高于L和BML組(P0.05或P0.01)。結(jié)論 BML-111抑制MAPK的磷酸化和NF-κB信號通路激活,并可能是其減輕VILI的機制之一。
[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- 偽 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- 偽 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.
【作者單位】： 華中科技大學(xué)同濟醫(yī)學(xué)院附屬協(xié)和醫(yī)院ICU;
【基金】：國家自然基金重點項目(No.30930089) 衛(wèi)生部臨床重點學(xué)科項目(2010-47)
【分類號】：R563

【共引文獻】

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1 忽新剛;佘守章;;呼吸機所致肺損傷治療的研究進展[J];贛南醫(yī)學(xué)院學(xué)報;2011年04期

2 代小奇;周華成;劉金鋒;張嘉航;鄧超;;全麻下經(jīng)口內(nèi)鏡下隧道術(shù)后并發(fā)癥早期發(fā)現(xiàn)及處理方法[J];哈爾濱醫(yī)科大學(xué)學(xué)報;2013年06期

相關(guān)博士學(xué)位論文 前4條

1 忽新剛;右旋美托咪啶對呼吸機所致肺損傷的保護作用及其機制研究[D];廣州醫(yī)學(xué)院;2011年

2 紀(jì)宇東;脂氧素受體激動劑BML-111抑制小鼠肺纖維化及相關(guān)機制研究[D];華中科技大學(xué);2013年

3 劉梅;阿司匹林誘生型脂氧素A4對小鼠急性肺損傷的保護作用及其機制研究[D];華中科技大學(xué);2013年

4 唐e，

本文編號：2110150