文章摘要
苏成磊,张华忠,陈俊杰,钱文溢,张劲松.硫化氢中毒对大鼠肺钠水主动转运功能的影响[J].南京医科大学学报,2014,(3):297~302
硫化氢中毒对大鼠肺钠水主动转运功能的影响
Alteration of ENaC-mediated alveolar fluid alearence by hydrogen sulfide intoxication
投稿时间:2013-11-08  
DOI:10.7655/NYDXBNS20140305
中文关键词: 硫化氢  α-上皮钠通道  肺泡液体清除率  ERK1/2
英文关键词: H2S  α-ENaC  alveolar fluid clearence  ERK1/2
基金项目:江苏高校优势学科建设工程资助项目(JX10231801)
作者单位
苏成磊 南京医科大学第一附属医院急诊科,江苏 南京 210029 
张华忠 南京医科大学第一附属医院急诊科,江苏 南京 210029 
陈俊杰 南京医科大学第一附属医院急诊科,江苏 南京 210029 
钱文溢 南京医科大学公共卫生学院神经毒理实验室,江苏 南京 210029 
张劲松 南京医科大学第一附属医院急诊科,江苏 南京 210029 
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中文摘要:
      目的:观察硫化氢(hydrogen sulfide,H2S)中毒对大鼠肺钠水主动转运功能的影响,并探讨其机制?方法:SD大鼠充分暴露于亚致命浓度(300 ppm)的H2S气体3 h,分别于暴露后6?12?24 h检测大鼠肺泡液体清除率(alveolar fluid clearance,AFC)和肺干湿比,光镜下观察肺组织HE染色,透射电镜下观察Ⅱ型肺泡上皮细胞的改变,real-time PCR检测肺组织α-上皮钠通道(epithelial sodium channel,ENaC)mRNA的表达,Western blot检测肺组织α-ENaC以及ERK1/2的蛋白表达?结果:SD大鼠暴露于H2S后,与对照组比较,AFC明显下降,在暴露后6 h最低;肺含水量在暴露后6 h最高,并在12 h恢复至正常水平;光镜下,暴露后24 h大鼠肺组织出现明显损伤性改变;大鼠Ⅱ型肺泡上皮细胞在暴露后出现线粒体脊断裂?板层小体崩解;大鼠肺组织中α-ENaC mRNA 在暴露后6 h表达增多,在12 h恢复至正常水平;α-ENaC的蛋白表达与对照组相比,则在暴露后6 h明显降低;大鼠肺组织ERK1/2磷酸化水平在暴露后6 h显著增高?结论:硫化氢中毒降低了大鼠AFC,其机制可能是下调了α-ENaC的表达,并且ERK1/2信号通路的激活可能参与了整个损伤过程?
英文摘要:
      Objective:To observe effects of hydrogen sulfide(H2S) intoxication on sodium and water transport function in rat lung and study its mechanism. Methods:SD rats were exposed to H2S gas with semi-lethal concentration(300 ppm) for 3 h. After 6 h,12 h and 24 h exposure to H2S,alveolar fluid clearence(AFC) and wet/dry ratio were measured. HE staining of lung tissues was observed by light microscope,and the change of type Ⅱ alveolar epithelial cells was observed by electron microscope. mRNA expression of α-epithelial sodium channel(ENaC) in the lung tissues was analyzed by real-time PCR. The expression of α-ENaC and ERK1/2 protein in the lung tissue was examined by Western blot . Results:After exposure to H2S, AFC was significantly decreased in SD rats compared to the control group, and reached a lowest level after 6 h and returned to a normal level after 12 h. The lung water content reached a lowest level after exposure for 6 h. Obvious injury changes of the lung tissue of rats were found after exposure for 24 h by light microscope. Dilated mitochondrial cristae and collapsed lamellar bodies were found in typeⅡalveolar epithelial cells of rats after exposure. The expression of α-ENaC mRNA in lung tissue was increased after exposure for 6 h and returned to a normal level after 12 h. Compared to the control group, the protein expression of α-ENaC was significantly decreased after exposure for 6 h. ERK1/2 dephosphorylation in lung tissues was significantly increased after exposure for 6 h. Conclusion:H2S intoxication decreases the AFC of rats and down-regulation of α-ENaC expression may be involved in as a potential mechanism. Furthermore, activated ERK1/2 signaling pathway may participate in the whole damaging process.
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