Effect of propofol on lymphocyte subsets and postoperative cognitive function in lung cancer model rats through JAK/STAT signaling pathway

Abstract

With changes in people’s living environment, the incidence of lung cancer is on the rise, seriously affecting people’s physical and mental health. Previous studies have shown that, propofol is used for treating lung cancer. Whether propofol affects lymphocyte subsets and postoperative cognitive function in rats with lung cancer remains unclear. In this study, we established and intervened rat lung cancer model, followed by Flow Cytometry/financal capacity model (FCM) analysis of peripheral blood lymphocyte subsets and apoptosis level. Morris water maze method was used to test cognitive function; while CCK-8 method and Transwell assessed tumor cells activities. qRT-PCR (Quantitative Real-time Polymerase Chain Reaction) and Western blot detected the expression of genes and proteins, respectively. Lung tissue of rats was swollen and alveolar damage was more serious, with tumor cell proliferation in high-dose propofol group being significantly inhibited with reduced migration ability and increased apoptosis. Moreover, Bcl-2 level in the JAK/STAT inhibitor group was lowest, and each lymphocyte subset index increased significantly, while the latency and swimming distance of rats decreased significantly. The expressions of JAK, STAT, and Bcl-2 mRNA in the high-dose propofol+JAK/STAT agonist group were significantly reduced. These expressions were directly regulated by propofol in the higher than high-dose propofol group (P <0.05), suggesting that propofol can directly regulate JAK, STAT, and Bcl-2. Propofol thus improves the lung cancer rats by inhibiting JAK/STAT signaling and down-regulating Bcl-2.