Study of inhibition of carbocisteine in airway mucin 1 of acute lung injury mice

Abstract

Objective To study the role of carbocisteine in inhibiting airway mucin 1 (Muc1) in acute lung injury (ALI) mice. Methods ALI mouse model was induced by lipopolysaccharide (LPS). C57 mice were randomly divided into four groups and respectively given the following treatments: saline by intranasal inhalation, carbocisteine by intraperitoneal injection, LPS by intranasal inhalation, LPS by intranasal inhalation combined with carbocisteine by intraperitoneal injection.The inflammatory cell number in bronchoalveolar lavage fluid (BALF) was counted.The expressions of Muc1 mRNA and protein were respectively detected by reverse transcription-polymerase chain reaction and Western blot.The level of tumor necrosis factor-α in BALF was detected by enzyme linked immunosorbent assay. Results Carbocisteine alone did not have effect on the inflammatory cell number in BALF.In BALF of ALI mice induced by LPS, the number of inflammatory cells was markedly increased, and most of them were neutrophils.Carbocisteine significantly inhibited the number of white blood cells and neutrophils (all P<0.05). In addition, carbocisteine significantly inhibited the expressions of Muc1 mRNA and protein.Carbocisteine significantly inhibited the level of tumor necrosis factor-α in BALF of ALI mice induced by LPS (P<0.05). Conclusions Carbocisteine can significantly inhibit airway inflammation and Muc1 expression of ALI mice. Key words: Carbocisteine; Mucin 1; Acute lung injury; Inhibition