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酸敏感离子通道-3在急性肺损伤大鼠肺组织中的表达
引用本文:邵兰,陈研生,徐少群,邱海波. 酸敏感离子通道-3在急性肺损伤大鼠肺组织中的表达[J]. 中华急诊医学杂志, 2009, 18(5). DOI: 10.3760/cma.j.issn.1671-0282.2009.05.005
作者姓名:邵兰  陈研生  徐少群  邱海波
作者单位:1. 东南大学附属中大医院ICU,南京,210009;广东省中医院
2. 广东省中医院
3. 东南大学附属中大医院ICU,南京,210009
基金项目:广东省医学科学研究基金 
摘    要:
目的 探讨酸敏感离子通道-3(ASIC3)在急性肺损伤肺组织中的表达.方法 24只雄性SD大鼠随机分为4组(每组6只):脂多糖(LPS)刺激组(LPS 2 h,LPS 4 h,LPS 6 h),分别为LPS刺激后2,4,6 h;生理盐水对照组;LPS组静脉注射LPS复制大鼠急性肺损伤模型,对照组静脉注射同等剂量生理盐水,以肺部特征性病理改变作为ALI模型成功的主要指标.各组检测动脉血气,留取肺组织标本,观察肺湿/干质量比、肺组织病理,免疫组化检测肺组织ASIC3的表达.统计数据用均数±标准差表示,采用SPSS 13.0统计软件行单因素方差分析、Dunnett-t检验和Kendall秩相关系数(Kendall'stau_b)检测其相关性,以P<0.05为差异具有统计学意义.结果 LPS 2 h,4 h,6 h组大鼠的动脉血氧分压(PaO2)分别为(67.47±6.01)mmHg,(59.17±7.18)mmHg,(52.54±7.62)mmHg,比对照组(98.15±1.06)mmHg低,差异有统计学意义(P<0.01);pH值LPS4 h(7.28±0.04),6 h(7.24±0.03)组显著低于对照组(7.35±0.01)(P<0.01).光镜下见肺组织内的炎性细胞逐渐增多,肺泡隔增宽,肺间质水肿,肺结构破坏逐渐加重;LPS注射后4 h,6 h肺泡上皮细胞内ASIC3的表达分别是(205.91±10.12),(196.51±18.60),显著低于对照组(220.23±10.11)(P<0.05);肺的湿/干质量比6 h组(5.18±0.21)亦明显高于对照组(4.45±0.18)(P<0.05).结论 LPS诱导的大鼠急性肺损伤肺泡上皮细胞和支气管黏膜上皮有ASIC3表达.

关 键 词:急性肺损伤  脂多糖  酸敏感离子通道-3

Expression of acid sensing ion channel 3 in the lung tissue of rats with, acute lung injury
SHAO Lan,CHEN Yan-sheng,XU Shao-qun,QIU Hai-bo. Expression of acid sensing ion channel 3 in the lung tissue of rats with, acute lung injury[J]. Chinese Journal of Emergency Medicine, 2009, 18(5). DOI: 10.3760/cma.j.issn.1671-0282.2009.05.005
Authors:SHAO Lan  CHEN Yan-sheng  XU Shao-qun  QIU Hai-bo
Abstract:
Objective To explore the expression of acid seining ion channels-3 (ASIC3) in lung tissue in rats with acute lung injury (ALI). Method Twenty four male Sprague-Dawley (SD) rats were randomly divided into four groups: LPS groups (LPS 2 h, LPS 4 h, LPS 6 h group, n=6), stimulated by LPS for 2, 4, 6 hours, respectively; normal control group, injected with saline (NS group, n=6). The ALI models were produced through venous injection of LPS, and the criteria was the characteristic pathological changes in the lung tissue. Ar-terial blood gas analysis was observed, lung wet and dry weight ratio (W/D), lung histopathology and ASIC3 ex-pression were detected. Data were expressed as mean±standard deviation. Independent Sample T test and One-way ANOVA and Kendall's tau_b were used for comparison in SPSS 13.0, and changes were considered as statistieal-ly significant if P value was less than 0.05. Results The partial pressure of oxygen (PaO2) in LPS 2 h, LPS 4 h, LPS 6 h group was (67.47±6.01), (59.17±7.18), (52.54±7.62) , respecively, and was significantly lower than that in eontrol group (98.15±1.06) (P<0.01). Compare with control group, pH was significantly lower in LPS4 h group (7.28±0.04), LPS6 h group (7.24±0.03) (P<0.01). Inflammation cells gradually increased, alveolar septum was widened, edema existed in interstitial spaces, and pulmonary structures gradually destroyed in LPS groups.The expression of ASIC3 in LPS4 h, LPS 6 h group was (205.91±10.12), (196.51± 18.60), respectively, and was significantly lower thanthat in control group (220.23±10.11) (P<0.05). The W/D in LPS 6 h group was (5.18±0.21), and was significantly higher than that in the control group (4.45± 0.18) (P<0.05). Conclusions ASIC3 is expressed in alveolar epithelial cells and bronchial epithehal cells in LPS-induced ALI rats.
Keywords:Acute lung injury  Lipopolysaccharide  Acid sensing ion channels-3
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