Objective:To observe alteration of expression of Gq/11 in lung injury during acute respiratory distress syndrome(ARDS) and propofol pre-treatment to explore the mechanism of Gq/11 signal transduction pathway and provide reference for the disease therapy. Methods: To establish an ARDS model in rats by intravenous olleic acid.48 male and healthy wistar rats were randomly divided into control group given equal volume normal saline(C, n=8), pre-treatment group received propofol at 100mg.Kg-1.h-1through left internal jugular vein for half hour before givene OA (0.2ml.Kg-1)(P, n=8)and oleic acid(OA, n=32)groups.According to time limit, OA groups were divided into 4 groups of OA30min,OA60min, OA90min,OA120min after injected OA at 0.2ml.Kg-1 though tail vein.Blood gas, plasma and lung homogenate ACE, LDH activity and MDA content were assessed during the experimental period and the concentration of Gq/11 were measured by Western blot. Results: Compared with control group, PaO2 of OA groups and pre-treatment group obviously decreased(P<0.01), but PaO2 of pre-treatment group was higher than that of OA groups(P<0.01). pH of OA30min group was higher than that of control group (P<0.05), furthermore OA 90min and OAl20min groups were markedly reduced(P<0.01). pH also reduced in Pre-treatment group, compared with control group (P<0.01), but was higher than that in OA 90min and OA120min groups(P<0.01). Plasma and lung homogenate ACE activity of OA groups and pre-treatment group were lower than those of control group and in decreasing tendency with time passing(p<0.01). To contrast with control group, the level of plasma and lung homogenate LDH and MDA of OA groups excluding OA30min group significantly increased(P<0.01) . There were no difference of indexof LDH in plasma and lung homogenate between pre-treatment group and control group, but pre-treatment group was lower than OA groups on the index(P<0.01). The concentration of plasma MDA of pre-treatment group was notably lower than those of OA groups, but great higher than those of control group(P<0.01). The concentration of lung homogenate MDA of pre-treatment group was higher ,compared with OA60min, OA90min, OA120min groups(p<0.01) and without difference with OA30min groups and control group.The MAP greatly decreased in OA groups and pre-treatment group as compared with that in control groupand MAP of pre-treatment group is lowest in all groups(p<0.01). In comparison with control group, the concentration of Gq/11 respectively increased (19.24 ± 2.38)%,(35.12 ±2.01%),(43.93 ± 1.62)%,(48.63 ± 1.88)% and (28.43 ± 2.67)% in OA groups and pre-treatment group with time passing (p<0.01). Gq/11 showed no significant discrepancy between pre-treatment group and OA30min group, while Gq/11 of pre-treatment group was obviously lower than those of OA60min, OA90min, OA120min groups(p<0.01). Conclusions: Up regulation of the expression of Gq/11 may play a role in ARDS lung injury. Pre-treatment with propofol can decrease the expression of Gq/11 in the lung tissue and relieve the injury of the lung during ARDS. |