Objective: To explore the effect of ulinastatin on anti-inflammation and pulmonary function protection with its mechanism for infants at cardiopulmonary bypass surgery. Methods: A total of 38 infants with ventricular septal defect undergoing cardiac operation were randomly divided into 2 groups. Ulinastatin group, the patients received uliastatin 20 000 U/kg,n=20 and Control group, the patients received the same volume of normal saline,n=18. The serum levels of TNF-α, IL-2, IL-l0 were examined at 4 time points: 5 min before skin incision (T1), immediate opening of aorta (T2), 4 hours after operation (T3) and 24 hours after operation (T4). The expressions of CD4+CD45+ T cells and CD4+Foxp3+ T cells were measured at T4. The respiratory index and oxygenation index at 4 time points were compared between 2 groups. Results: Compared with Control group, Ulinastatin group had the lower levels of TNF-α, IL-2 and higher level of IL-l0 at T2, T3, T4; Ulinastatin group also had the higher oxygenation index and lower respiratory index at T2, T3, T4, allP<0.05. Ulinastatin group had less expression of CD4+CD45+ T cells (35.98 ± 3.67)% than Control group (41.94 ± 4.56)% , and more expression of CD4+Foxp3+ T cells (19.65 ± 3.45)% than Control group (6.45 ± 1.47)%,P<0.05-P<0.01. Conclusion: Ulinastatin may improve the differentiation from CD4+CD45+ T cell to Foxp3+CD4+ T cell, down regulating inlfammatory response and protecting pulmonary function for infants at cardiopulmonary bypass surgery.

Objective: To investigate the effects of combined exposure to black carbon and lead on the expression of cell adhesion molecules and their regulating microRNAs (miRNAs) in the rat choroid plexus epithelial Z310 cells. Methods: i) Z310 cells were randomly divided into control group, black carbon exposure group, lead exposure group and combined exposure group. The lead exposure group and black carbon exposure group were treated with 10 μmol/L lead acetate and 10 mg/L black carbon, respectively, and the combined exposure group was treated with both in the above doses. After 12.0 hours, the expressions of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and mucosal vascular addressin cell adhesion molecule-1 (MAdCAM-1) in Z310 cells was detected by Western blotting. The expression of miR-326, miR-328-3p and miR-542-3p which regulated ICAM-1 was detected by real-time fluorescent quantitative polymerase chain reaction. ii) Z310 cells or Z310 cells transfected with miRNA-326 mimic were randomly divided into control group, miRNA-326 transfection control group, combined exposure group and miRNA-326 transfection combined exposure group. Cells in the two control groups were not treated. The two combined exposure groups were treated with 10 mg/L black carbon and 10 μmol/L lead acetate for 12.0 hours. The expression of ICAM-1 was detected by Western blotting. Results: i) The relative expression of ICAM-1, VCAM-1 and MAdCAM-1 in the cells of black carbon exposure group and ICAM-1 in the lead exposure group was higher than those in the control group (all P<0.05). The relative expression of ICAM-1 and MAdCAM-1 in the combined exposure group was higher than those in the other three groups (all P<0.05). The relative expression of VCAM-1 in cells of combined exposure group was higher than those in the control group and lead exposed group (all P<0.05). The relative expression of miR-326 in cells of the lead exposure group and black carbon exposure group was lower than those in the control group (all P<0.05). The relative expression of miR-326 in the combined exposure group was lower than that in the other three groups (all P<0.05). There was no significant difference between miR-328-3p and miR-542-3p in the four groups (all P>0.05). ii) The relative expression of ICAM-1 in cells of the miR-326 transfection control group cells was lower than that in the control group (P<0.05), while in the cells in the combined exposure and miRNA-326 transfection combined exposure group, it was higher than that in the control and miRNA-326 transfection control groups (all P<0.05), and lower in the miRNA-326 transfection combined exposure group than in the combined exposure group (P<0.05). Conclusion: Black carbon or lead exposure can upregulate the expression of ICAM-1, VCAM-1 and MAdCAM-1 in Z310 cells. Black carbon and lead combined exposure lead to a synergistic effect on upregulation of ICAM-1 and MAdCAM-1 expression, particularly ICAM-1. The combined exposure of black carbon and lead may upregulate the expression of ICAM-1 by downregulating the expression of miR-326.