Sevoflurane attenuates ventilator­induced lung injury by regulating c­PLA2 expression.

The aim of the present study was to investigate the potential role of club cell secretory protein (CCSP), an endogenous modulator, in reducing pulmonary inflammation induced by sevoflurane following one­lung ventilation (OLV). Healthy Japanese white rabbits were randomly assigned to six groups: Sham­operated group (group S); respiratory management of OLV group (group O); OLV + sevoflurane treated group (group OF), club cells exfoliated + sham­operated group (group NA), club cells exfoliated + OLV group (group NAO); and club cells exfoliated + OLV + sevoflurane treated group (group NAOF). At the end of the experimental observation, all animals in the different groups were sacrificed and lung injury was evaluated according to the lung wet/dry weight ratio and histological scoring system. Lung homogenates were harvested to detect the mRNA and protein expression of cytosolic phospholipase A2 (c­PLA2) and CCSP. The content of arachidonic acid was measured using an ELISA. Following OLV treatment, c­PLA2 expression was increased, CCSP expression was decreased and lung injury scores were significantly increased. Sevoflurane inhalation in the OLV­treated group induced an upregulation of CCSP and a downregulation of c­PLA2 expression. In the group NAO, in which the club cells were simultaneously exfoliated, OLV caused more severe lung damage and induced higher expression of c­PLA2 compared with that in group O. However, sevoflurane inhalation reduced the extent of lung injury and the expression of c­PLA2, even when the endogenous modulator of lung inflammation, CCSP, was exfoliated (group NAOF). These results indicated that OLV promoted lung inflammation through the CCSP and c­PLA2 pathway. However, the results from the club cells exfoliated group indicated that the CCSP may not be involved in the protective effect exerted by sevoflurane inhalation.