Abstract:

Objective To investigate the function of proinflammatory cytokines in the animal model of fat embolism syndrome and its potential signal transduction pathways. Methods The fat embolism model was established by injection with the allogeneic perinephric fat through the caudal veins of healthy male C57BL mice. The half lethal dose (LD50) was calculated by Bliss´ method. Mice in experiment group were injected with LD50 of fat, and those in control group were managed with the same dose of normal saline. The lung tissue damage (both gross and microscope), arterial blood gas, ratio of lung tissue wet and dry weight (D/W), activity of myeloperoxidase (MPO) in lung tissues, plasma IL-1β and TNF-α levels and expression of IKK β gene and NF-κB protein in lung tissue homogenate were compared between groups. Results Compared with control group, the lung tissues were seriously damaged, there was lipid droplet accumulation in the endovascular and alveolar space, and D/W increased in experiment group. In experiment group, the arterial oxygen partial pressure (PaO₂) significantly decreased, the arterial carbon dioxide partial pressure (PaCO₂) increased, plasma IL-1β and TNF-α significantly increased, the activity of MPO in lung tissues enhanced, and the expression of IKKβ gene and NF-κB increased (P<0.05). Conclusion Inflammatory reaction plays an important role in the pathological process of fat embolism syndrome, and the increase of NF-κB related gene and protein indicates the participation of the inflammatory signal pathways mediated by NF-κB.

Key words: fat embolism syndrome, lethal dose 50, animal model, proinflammatory cytokine, signal transduction pathway