Abstract:

Objective To investigate the protective effect of lytic cocktail on lung tissues of severely scalded rats at the initial stage, and explore the potential mechanism. Methods Sixty-six male SD rats were randomly divided into sham scald group (n=6, sham scald with subcutaneous injection of 12 mL/kg saline), scald group (n=30, third degree scald with subcutaneous injection of 12 mL/kg saline) and scald+lytic cocktail group (n=30, third degree scald with subcutaneous injection of 12 mL/kg lytic cocktail). Blood samples were obtained 3 h after scald simulation from sham scald group and 3 h, 6 h, 12 h, 24 h and 48 h after scald from scald group and scald+lytic cocktail group, and lung tissues were harvested after sacrifice from each group. Plasma levels of interleukin 1β (IL-1β), tumor necrosis factor α (TNF-α), interleukin 10 (IL-10), soluble intercellular adhesion molecule 1 (sICAM-1) and endothelin 1 (ET-1) were determined with ELISA, and the activity of myeloperoxidase (MPO) and the expression of CD68 in lung tissues were detected with enzymatic spectrophotometry and immunohistochemistry, respectively. Pathological changes in lung tissues were observed under light microscope with HE staining. Results The plasma levels of IL-1β, TNF-α, sICAM-1 and ET-1, and the activity of MPO and the expression of CD68 in lung tissues in scald+lytic cocktail group were higher than those in sham scald group and lower than those in scald group. The plasma level of IL-10 in scald group was higher than that in sham scald group and lower than that in scald+lytic cocktail group. There were significant differences in part of the above parameters among groups （P<0.05 or P<0.01）. Compared with scald group 24 h after scald, pulmonary interstitial edema in scald+lytic cocktail group was alleviated at the corresponding time point. Conclusion Lytic cocktail can effectively alleviate the pulmonary interstitial edema and inflammation of lung tissues of severely scalded rats at the initial stage, and the potential mechanism may relate to the regulation of inflammation and reduction in activation and injury of endothelial cells.

Key words: burn, endothelial cell, lung, lytic cocktail, inflammatory response