AIM: To examine expression of macrophage migration inhibitroy factor (MIF) gene and protein in macrophages induced by oxidized low density lipoprotein (ox-LDL). METHODS: Macrophages were incubated with ox-LDL at the concentration of 150 mg/L for time course (0-36 h) and with ox-LDL at the different concentrations (0-300 mg/L) for 24 h, expression of MIF mRNA and protein were detected by RT-PCR and ELISA. RESULTS: The results showed that ox-LDL increased MIF gene and protein expression in macrophages in a dose and time-dependent manner. After the exposure of macrophage to ox-LDL, the expression of MIF mRNA level increased consistently with protein. CONCLUSION: MIF may play an important role in atherosclerosis. [

Objective To evaluate the protective effect on lung by using continuous pulmonary artery perfusion with oxygenated blood and L-arginine during cardiopulmonary bypass(CPB).Methods Forty five cases received mitral valve replacement were randomly divided into 3 groups and each group involved 15 cases. Group I(control group), patients received routine procedure of CPB. Proup Ⅱ, patients received rcontinuous pulmonary artery perfusion with oxygenated blood. Group Ⅲ,continuous pulmonary artery perfusion with oxygenated blood containing L-arginine (200 mg/kg) (n=15). All cases received routine procedure of CPB and continuously infused from the root of pulmonary artery until releasing aortaoaic clamp. Blood samples were collected from the radial artery respectively at the following time points:after the induction of anaesthesia, 1 hour after opening of aorta, 0, 6, 12, 24 hours after patients being taken back to ICU. ELISA test was used to detected the expression of tmmor necrosis factor-α(TNF-α), interleukin-6 (IL-6) and interleukin-10 (IL-10). Lung tissue samples (1.0 cm ×1.0 cm×1.0 cm) were obtained from right lower lobe. The pathologicl changes of lung tissues were observed under light mi-croscope by using HE staining. Results at each time points, the expression of TNF-α, IL-6 in group Ⅱ and group Ⅲ weresignificantly lower than that in group Ⅰ (P<0.05). The level of TNF-α, IL-6 in group Ⅲ were lower than in group Ⅱ(P<0.05). However, the expression of IL-10 in group Ⅱ and group Ⅲ were higher than in group Ⅰ, and the level of IL-10 in group Ⅲ were higher than that in group Ⅱ(P<0.05). In the group Ⅰ: HE staining showed marked pulmonary interstitial edema, intra-alveolus neutrophilic granulocyte exudation with karyorrhexis. In the group Ⅱ, light capillary vessel hyperaemia and pulmonary interstitial lymphocyte exudation were detected. Nearly normal lung tissue were observed in group Ⅲ. Conclusion Continuous pulmonary artery perfusion with oxygenated blood and L-arginine could inhibit the synthesis of inflammatory factors significantly and increase the releasing of anti-inflammatory factors during CPB. Therefore, it may reduces pulmonary inflammatory reaction and have protective effects on lung tissue.