Open AccessKeratinocyte growth factor‐2 intratracheal instillation significantly attenuates ventilator‐induced lung injury in rats
Author(s) -
Bi Jing,
Tong Lin,
Zhu Xiaodan,
Yang Dong,
Bai Chunxue,
Song Yuanlin,
She Jun
Publication year - 2014
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.12269
Subject(s) - keratinocyte growth factor , lung , bronchoalveolar lavage , tumor necrosis factor alpha , medicine , inflammation , pulmonary surfactant , surfactant protein a , pathology , andrology , immunology , growth factor , biology , receptor , biochemistry
Preservation or restoration of normal alveolar epithelial barrier function is crucial for pulmonary oedema resolution. Keratinocyte growth factor‐2 ( KGF ‐2), a potent epithelial cell mitogen, may have a role in preventing ventilator‐induced lung injury ( VILI ), which occurs frequently in mechanically ventilated patients. The aim of the study was to test the role of KGF ‐2 in VILI in rats. Forty healthy adult male S prague‐ D awley rats were randomly allocated into four groups, where rats in Groups HVZP (high‐volume zero positive end‐expiratory pressure) and HVZP + KGF ‐2 were given intratracheally equal PBS and 5 mg/kg KGF ‐2 72 hrs before 4 hrs HVZP ventilation (20 ml/kg), respectively, while PBS and KGF ‐2 were administered in the same manner in Groups Control and KGF ‐2, which underwent tracheotomy only with spontaneous breathing. Inflammatory cytokines (tumour necrosis factor‐α, macrophage inflammatory protein 2), neutrophil and total protein levels in bronchoalveolar lavage fluid and surfactant protein m RNA expression in lung tissue were detected; the number of alveolar type II cells, lung water content and lung morphology were also evaluated. The results indicate that pre‐treatment with KGF ‐2 showed dramatic improvement in lung oedema and inflammation compared with HVZP alone, together with increased surfactant protein m RNA and alveolar type II cells. Our results suggest that KGF ‐2 might be considered a promising prevention for human VILI or other acute lung injury diseases.