Caspase-9 and p53 Protein Levels in Cancer Patients after Different Anesthesia Techniques

The aim of this study was to investigate the changes in caspase-9 and p53 levels as biomarkers of pro- and anti-apoptotic pathways in the early postoperative period in patients who underwent lung surgery for malig-nant tumors under different types of multimodal or inhalation-intravenous anesthesia. Material and Methods. A single-center prospective study of 22 patients aged 45–64 years was conducted at the Omsk Clinical Oncology Early Treatment and Prevention Center from January to April 2020. The participants were divided into two groups. Group 1 patients received multimodal anesthesia, which included sympathetic nerve block and prolonged epidural analgesia in the postoperative period. Group 2 patients received inhalational and intravenous anesthesia followed by systemic morphine analgesia. Serum caspase-9 and p53 protein levels were measured at four time points: before anesthesia, one, twelve, and twenty-four hours after surgery. Statistical hypotheses were tested using nonparametric (rank) analysis methods. Friedman's ANOVA was used to compare multiple time points, while the Wilcoxon test was used to compare variables between two time points in dependent samples. The Mann-Whitney test was used to assess differences between groups in independent samples. P-values < 0.05 were considered statistically significant. Results are expressed as median ± half interquartile range (Me ± (LQ – UQ) / 2). Results. At time point 2, caspase-9 levels were significantly higher in group 2 patients than in group 1 (P = 0.045). There were no significant differences between the groups at any other time points. Conclusion. The lack of a significant difference in serum levels of caspase-9 and p53 protein at most time points between the groups demonstrates the efficacy of the anesthesia and analgesia methods used. Mean-while, a significantly higher level of caspase-9 one hour after surgery demonstrates a greater susceptibility of patients without sympathetic blockade to activation of the apoptotic cell death program.