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 2h,LPS 4h,LPS 6h),分别为IPS刺激后2,4,6h;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SPSS13.0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LPS2h,4h,6h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LPS4h(7.28±0.04),6h(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4h,6h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6h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。
Objective To explore the expression of acid sensing 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. Arterial 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 tan_ 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 control group (98.15 ± 1.06) (P 〈 0.01). Compare with control group, pH was significantly lower in LPS g h group (7.28 ± 0.04 ), LPS 6 h group (7.24 ± 0.03) ( P 〈 0.01 ). Inflammation ceils gradually increased, alveolar septum was widened, edema existed in interstitial spaces, and pulmonary structures gradually destroyed in LPS groups. The expression of ASIC3 in LPS 4 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 epithelial cells in LPS-induced ALI rats.
出处
《中华急诊医学杂志》
CAS
CSCD
北大核心
2009年第5期466-470,共5页
Chinese Journal of Emergency Medicine
基金
广东省医学科学技术研究基金资助项目(WSTJJ2004122843040419710323001X)
关键词
急性肺损伤
脂多糖
酸敏感离子通道-3
Acute lung injury
Lipopolysaccharide
Acid sensing ion channels-3