Background The present study is aimed to explore the role and mechanism of gastric acidified pepsin in promoting laryngeal *** In vitro and in vivo,the effect of acidified pepsin on H+/K+-ATPase,autophagy/mitophagy of...
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Background The present study is aimed to explore the role and mechanism of gastric acidified pepsin in promoting laryngeal *** In vitro and in vivo,the effect of acidified pepsin on H+/K+-ATPase,autophagy/mitophagy of mouse laryngeal epithelial cells was detected by haematoxylin-eosin staining,IHC,CCK8,flow cytometry assays,TUNEL staining,Western Blotting,quantitative real-time PCR,immunofluorescence and transmission electron microscope(TEM).The expression of H+/K+-ATPase α,β-subunits,pepsin in 31 human specimens of normal laryngeal mucosa obtained from laryngocarcinoma patients were analysis by immunohistochemical staining(IHC).results Acidified pepsin(pH3) promoted cell viability and the proportion of S-phase laryngeal epithelial cells in vitro and induced the thickness of mucosa,and cell growth of laryngeal epithelial cells in ***,especially mitophagy,was activated,while mitochondrial membrane potential(MMP) was inhibited after exposure with *** contrast,autophagy inhibited by chloroquine(CQ) abolished acidified pepsin-induced mitophagy and cell viability of laryngeal epithelial *** administration induced cell apoptosis and enlarged the decline of MMP in the presence of pepsin in acidic *** was relationship between H+/K+-ATPase β and α,between H+/K+-ATPase β and pepsin.H+/K+-ATPase knockout or inhibition using pantoprazole further reduced MMP in the presence of acidified pepsin in *** of cell proliferation was mediated by acidified pepsin by upregulating cell apoptosis in vitro and/or in *** In acidic environment,pepsin can upregulate cell viability of laryngeal epithelial cells by activating mitophagy and reducing mitochondria damage via elevating H+/K+-ATPase expression,leading to laryngeal precancerosis.
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