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首页> 外文期刊>American Journal of Translational Research >Pendrin, an anion exchanger on lung epithelial cells, could be a novel target for lipopolysaccharide-induced acute lung injury mice
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Pendrin, an anion exchanger on lung epithelial cells, could be a novel target for lipopolysaccharide-induced acute lung injury mice

机译：Pendrin是肺上皮细胞上的阴离子交换剂，可能是脂多糖诱导的急性肺损伤小鼠的新靶标

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Objective: The aim of this study is to evaluate the role of pendrin in acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) and to explore whether pendrin expression existing on alveolar cells. Methods: ALI C57BL/6 mice model induced by lipopolysaccharide (LPS) was established. The expression of pendrin in lung was analyzed by RT-PCR and western blotting methods, the changes of lung inflammatory parameters and pathology were observed, the cellular distribution of pendrin in the lung was determined using immunofluorescence. Statistical comparisons between groups were made by two-tailed Student’s t-test. Results: Enhanced expression of the slc26a4 gene and production of pendrin in lungs of LPS-induced ALI mice were confirmed. In comparison with vehicle-control mice, methazolamide treatment mitigated lung inflammatory parameters and pathology. IL-6 and MCP-1 in lung tissues and BALF in methazolamide-treated mice were statistically decreased. Methazolamide treatment had significant effect on the total protein concentration in the BALF and the ratio of lung wet/dry weight. The percentage of macrophages in the BALF was increased. There was a low expression of pendrin in ATII. Conclusions: Pendrin may be involved in pathological process of LPS-induced ALI. Inhibition of the pendrin function could be used to treat ALI. Airway epithelial cell may be a valuable therapeutic target for discovering and developing new drugs and/or new therapeutic strategies for the treatment of ALI/ARDS.
机译：目的：本研究旨在评估Pendrin在急性肺损伤（ALI）/急性呼吸窘迫综合征（ARDS）中的作用，并探讨pendrin在肺泡细胞上的表达是否存在。方法：建立脂多糖（LPS）诱导的ALI C57BL / 6小鼠模型。采用RT-PCR和Western blotting方法分析肺中Pendrin的表达，观察肺炎性参数和病理的变化，采用免疫荧光法测定肺中Pendrin的细胞分布。两组之间的统计比较是通过两尾学生t检验进行的。结果：证实了LPS诱导的ALI小鼠肺中slc26a4基因的表达增强和Pendrin的产生。与媒介物对照小鼠相比，甲唑胺治疗减轻了肺部炎症参数和病理。肺组织中的IL-6和MCP-1以及甲唑酰胺治疗的小鼠中的BALF均有统计学下降。甲唑酰胺处理对BALF中总蛋白浓度和肺干/湿重之比有显着影响。 BALF中巨噬细胞的百分比增加。在ATII中Pendrin的表达较低。结论：Pendrin可能参与了LPS诱导的ALI的病理过程。 Pendrin功能的抑制可用于治疗ALI。气道上皮细胞可能是发现和开发新药物和/或治疗ALI / ARDS的新治疗策略的重要治疗靶标。

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