Found programs:
Authors:Zhu Yueqin; Pan Xuesheng; Du Na
Keywords:acute lung injury;acid-sensitive ion channels;lipopolysaccharide;amiloride;endoplasmic reticulum stress
DOI:10.19405/j.cnki.issn1000-1492.2020.03.014
〔Abstract〕 Objective To investigate the effect of acid-sensitive ion channel-1 a on the expression of endoplasmic reticulum stress-related protein in rats with acute lung injury induced by lipopolysaccharide(LPS).Methods 40 SPF male Sprague Dawley rats weighing 180~220 g were randomly divided into 4 groups(10 in each group): Control group, Model group, Amiloride group and Dexamethasone(Dex) group. The pathological changes of lung tissue were observed in rats, and the expression of interleukin-6(IL-6) in serum was detected by ELISA. The expres-sion levels of glucose-regulated protein 78(GRP78), C/EBP-homologous protein(CHOP), Inositol-requiring kinase 1( IRE-1) and X box binding protein 1( XBP-1) were detected by Real-time quantitative PCR. GRP78,ccaspase-12,IRE-1α and XBP-1 in lung tissue were detected by Western blot. Results Compared with the Control group,lung tissues in the Model group showed alveolar collapse and interstitial edema; the expression of IL-6 was up-regulated( P<0. 01). The expression of indicators related to lung tissue decreased in the amiloride group and the Dex group. Western blot results showed that the protein expression of endoplasmic reticulum stress-related genes in the Model group was increased compared with the Control group,and the protein expression of endoplasmic reticulum stress-related genes in the Amiloride group was lower than that in the Model group( P<0. 01). Real-time quantitative PCR results showed that the mRNA expression of endoplasmic reticulum stress-related genes in the Model group was increased compared with the Control group,and the mRNA expression of endoplasmic reticulum stress-related genes in the Amiloride group was lower than that in the Model group( P<0. 01). Conclusion Upregulation of ASIC1 a in LPS-induced acute lung injury rats may mediate endoplasmic reticulum stress response.