氯化釓對(duì)膿毒癥大鼠急性肺損傷的肺保護(hù)作用
發(fā)布時(shí)間：2019-05-12 20:29
【摘要】：目的建立大鼠膿毒癥急性肺損傷模型，探討氯化釓（GdCl3）在膿毒癥大鼠急性肺損傷中的肺保護(hù)作用及可能機(jī)制，為臨床治療膿毒癥急性肺損傷提供新的理論和實(shí)驗(yàn)依據(jù)。 方法采用盲腸結(jié)扎穿孔術(shù)（CLP）建立膿毒癥急性肺損傷模型。將36只成年Wistar大鼠采用10%水合氯醛0.3g/Kg腹腔注射麻醉后，行正中切口開腹，暴露盲腸，隨即均分為假手術(shù)組(Sham組)、膿毒癥組（CLP組）和氯化釓治療組（GdCl3組），每組12只，CLP組和GdCl3組于盲腸根部絲線結(jié)扎，盲腸切口5mm，腸內(nèi)容物漏出，將其回納入腹腔，關(guān)腹。假手術(shù)組大鼠僅翻動(dòng)盲腸，不結(jié)扎穿孔。GdCl3組術(shù)后經(jīng)尾靜脈注射2%GdCl3溶液（10mg.kg-1）。實(shí)驗(yàn)結(jié)束后，，應(yīng)用酶聯(lián)免疫法（ELISA）法測(cè)定血漿中腫瘤壞死因子α（TNF-α）水平，應(yīng)用硫代巴比妥酸（TBA）法測(cè)定丙二醛(MDA)水平，測(cè)定肺濕／干重比值（W/D）,部分肺組織用HE染色法染色并在光鏡下觀察肺組織病理結(jié)構(gòu)的改變，統(tǒng)計(jì)方法采用SPSS19.0。 結(jié)果與Sham組相比， CLP組、GdCl3組血漿TNF-α、MDA水平，W/D明顯升高，差異有統(tǒng)計(jì)學(xué)意義（P＜0.05）；與CLP組相比， GdCl3組血漿TNF-α、MDA水平，W/D明顯降低，差異有統(tǒng)計(jì)學(xué)意義（P＜0.05）;肺病理提示CLP組和GdCl3組肺泡間隔及肺泡內(nèi)炎性細(xì)胞浸潤(rùn)、出血， GdCl3組肺組織病理學(xué)改變明顯減輕。 結(jié)論急性肺損傷時(shí)，血漿TNF-α、MDA水平明顯升高，GdCl3可通過抑制巨噬細(xì)胞釋放的TNF-α等炎性介質(zhì)來減輕膿毒癥所致的急性肺損傷的炎癥反應(yīng)。
[Abstract]:Objective to establish a rat model of acute lung injury induced by sepsis and to explore the protective effect and possible mechanism of gadolinium chloride (GdCl3) in acute lung injury in septic rats, so as to provide a new theoretical and experimental basis for clinical treatment of acute lung injury with sepsis. Methods the acute lung injury model of sepsis was established by cecal ligation and perforation (CLP). Thirty-six adult Wistar rats were anesthetized with 10% chloral hydrate 0.3g/Kg intraabdominal injection, then underwent median incision laparotomy and exposed cecum. They were divided into three groups: sham operation group (Sham group), sepsis group (CLP group) and gadolinium chloride treatment group (GdCl3 group). In each group, 12 rats in CLP group and GdCl3 group were ligated at the root of cecum, the cecum incision was 5 mm, the intestinal contents leaked out, and the contents of the intestine were returned to the abdominal cavity and closed the abdomen. Rats in the sham operation group only turned the cecum without ligating and perforation. 2%GdCl3 solution (10mg.kg-1) was injected intravenously through the tail vein after operation in the GdCl3 group. At the end of the experiment, the level of tumor necrosis factor 偽 (TNF- 偽) in plasma was measured by enzyme linked immunosorbent assay (Elisa), the level of malondialdehyde (MDA) (MDA) was measured by thiobarbituric acid (TBA) method, and the lung wet / dry weight ratio (W 鈮
本文編號(hào)：2475681
[Abstract]:Objective to establish a rat model of acute lung injury induced by sepsis and to explore the protective effect and possible mechanism of gadolinium chloride (GdCl3) in acute lung injury in septic rats, so as to provide a new theoretical and experimental basis for clinical treatment of acute lung injury with sepsis. Methods the acute lung injury model of sepsis was established by cecal ligation and perforation (CLP). Thirty-six adult Wistar rats were anesthetized with 10% chloral hydrate 0.3g/Kg intraabdominal injection, then underwent median incision laparotomy and exposed cecum. They were divided into three groups: sham operation group (Sham group), sepsis group (CLP group) and gadolinium chloride treatment group (GdCl3 group). In each group, 12 rats in CLP group and GdCl3 group were ligated at the root of cecum, the cecum incision was 5 mm, the intestinal contents leaked out, and the contents of the intestine were returned to the abdominal cavity and closed the abdomen. Rats in the sham operation group only turned the cecum without ligating and perforation. 2%GdCl3 solution (10mg.kg-1) was injected intravenously through the tail vein after operation in the GdCl3 group. At the end of the experiment, the level of tumor necrosis factor 偽 (TNF- 偽) in plasma was measured by enzyme linked immunosorbent assay (Elisa), the level of malondialdehyde (MDA) (MDA) was measured by thiobarbituric acid (TBA) method, and the lung wet / dry weight ratio (W 鈮
本文編號(hào)：2475681
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