Abstract

To observe the protective effect of insulin-like growth factor-1 (IGF-1) on acute lung injury induced by perfluoroisobutylene (PFIB) inhalation in mice. Sixty-four male Kunming mice were randomly divided into normal control (A) group, exposed (B) group, recombinant adenoviruses 5 of IGF-1 (Ad5-IGF-1) intervention (C) group (in which Ad5-IGF-1 was injected into the trachea of the mice), blank vector control (D) group. B, C and D groups were exposed to gaseous PFIB in a flow-past whole-body exposure system. The lung index, concentration of total protein and albumin in bronchoalveolar lavage fluid (BALF), concentration of IGF-1 in serum and lung homogenate were measured. The lung pathologic changes were examined with light microscope, and ultrastructure changes in alveolar type II cells (ATII) with electron microscope. Compared with A group, the lung index, concentration of total protein in BALF were significantly increased in other groups, the lung index and concentration of total protein and albumin of BALF in B and D groups were prominently higher than C group (all P<0.01). The concentration of IGF-1 in serum of B and D groups was lower markedly than that of A group, and the concentration of IGF-1 in serum of C group was distinctly higher than those of A, B, D groups (all P<0.01). The concentration of IGF-1 in lung homogenate of B, C, D groups was higher than that of A group, and the concentration of IGF-1 in lung homogenate of C group was significantly higher than that of B and D groups (all P<0.01). Lung hyaline membrane formation, diffuse alveolar atelectasis, accumulation of edema fluid, red blood cell exudation, were obviously milder in C group, and changes in the ultrastructure of ATII showed a similar result. The protective effect of Ad5-IGF-1 against the toxicity of PFIB inhalation is identified. In the mice pretreated with Ad5-IGF-1 is able to significantly lower lung index, the protein concentration in BALF, and the concentration of IGF-1 in serum and lung homogenate is obviously increased. Protection of ATII may be one of the mechanisms.

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