Author contributions: Ma JJ carried out the Adhesion assays, drafted the manuscript and participated in the design of the study; Feng B carried out the molecular expression studies, and in vitro pneumoperitoneum establishment; Zhang Y carried out the cell invasive assay; Li JW participate in the induction of intra-abdominal tumors; Lu AG participated in the molecular expression studies; Wang ML performed the statistical analysis; Peng YF, Hu WG, Yue F participated in the cell invasive assay; Zheng MH conceived of the study, and participated in its design and coordination and helped to draft the manuscript.
METHODS:With an in vitro artificial pneumoperitoneum model, SW1116 human colon carcinoma cells were exposed to CO2-insufflation in 5 different pressure groups: 6 mmHg, 9 mmHg, 12 mmHg, 15 mmHg and control group, respectively for 1 h. Expression of E-cadherin, ICAM-1, CD44 and E-selectin was measured at 0, 12, 24, 48 and 72 h after CO2-insufflation using flow cytometry. The adhesion and invasion capacity of SW1116 cells before and after exposure to CO2-insufflation was detected by cell adhesion/invasion assay in vitro. Each group of cells was injected intraperitoneally into 16 BALB/C mice. The number of visible abdominal cavity tumor nodules, visceral metastases and survival of the mice were recorded in each group.
RESULTS:The expression of E-cadherin, ICAM-1, CD44 and E-selectin in SW1116 cells were changed significantly following exposure to CO2 insufflation at different pressures (P < 0.05). The expression of E-cadherin, CD44 and ICAM-1 decreased with increasing CO2-insufflation pressure. The adhesive/ invasive cells also decreased gradually with increasing pressure as determined by the adhesion/invasion assay. In animal experiments, the number of abdominal cavity tumor nodules in the 15 mmHg group was also significantly lower than that in the 6 mmHg group (29.7 ± 9.91 vs 41.7 ± 14.90, P = 0.046). However, the survival in each group was not statistically different.
CONCLUSION: CO2-insufflation