Effect of Propofol on Expression of PKC mRNA in Pulmonary Injury Induced by Ischemia-Reperfusion in Rabbits

Abstract

Aim: This prospective study aimed at investigating the effect of propofol on the expression of protein kinase C (PKC) mRNA during pulmonary ischemia-reperfusion injury (PIRI) in the rabbits. Methods: Single lung ischemia-reperfusion animal model was administrated in vivo. The rabbits were randomly divided into three groups): sham-operated group (Sham); pulmonary I/R group (PIR) and PIR+propofol group (PIR+PPF). Changes of several parameters, including malondialdehyde (MDA) concentration, superoxide dismutase (SOD) activity, nitric oxide (NO) content, wet/dry ratio of lung tissue (W/D) and the index of quantitative assessment of histologic lung injury (IQA) were measured at 60 min after reperfusion. Meanwhile, the location and expression of PKC mRNA were observed, lung tissues were also harvested for histopathological evaluation. Results: As compared with PIR group, PKC mRNA is largely expressed in intima and extima of small pulmonary artery as well as thin-wall vessels (mostly small pulmonary veins). The average optical density values of PKC-α, δ and θ mRNA in small pulmonary veins in PIR+PPF group showed obviously higher than that in group PIR (all P<0.01); the activity of SOD increased, the concentration of MDA, W/D and IQA decreased at 60 min after reperfusion in lung tissue (P<0.01 and P<0.05). Abnormal morphological changes of the lung tissue were lessened markedly in PIR+PPF group. Conclusions: The results of this study suggested that propofol possesses and acts its notable protective effect on PIRI in rabbits by activating PKC-α, δ and θ mRNA expression in lung tissue, raising NO level, reducing OFR level and decreasing lipid peroxidation.