[Activity of nuclear factor kappa B in rat pulmonary tissue after entrance of amniotic fluid into blood and inhibition with dexamethasone].

OBJECTIVE

To investigate the relationship between nuclear factor kappa B (NF-kappaB) and pulmonary injury in amniotic fluid embolism model of rat.

METHODS

Seventy female Wistar rats were divided into five groups randomly: control group (6), amniotic fluid group (16), amniotic fluid + dexamethasone group (14), meconium group (20) and meconium + dexamethasone group (14). Different amniotic fluid was injected into jugular vein (dexamethasone was injected at 0.1 mg/100 g after entrance of amniotic fluid into blood) and blood pressure was examined. Pulmonary tissue was taken at 60 minutes. NF-kappaB activity was measured by Western-blot and percentage of NF-kappaB p65 positive cells in pulmonary tissue was determined by immunohistochemistry (HE).

RESULTS

Dropsy, bleeding and neutrophil (PMN), macrophage, leukomonocyte infiltration were seen in four experimental groups. But none was found in control group. NF-kappaB activity in meconium group was 438,698 +/- 13,092, higher than those in amniotic fluid group, 377,982+/- 7,445, and in control group, 267,691 +/- 12 382 (F = 11.3, P < 0.01). With dexamethasone treatment, NF-kappaB activity was decreased, which was 308,826 +/- 13,771 in amniotic group and 339,516 +/- 17,358 in meconium group, respectively (t = 20.4 and t = 13.84, P < 0.01). Percentage of NF-kappaB p65 positive cells was higher in meconium group, 49.1 +/- 7.0, than in amniotic fluid group, 33.3 +/- 2.7, and control group, 13.3 +/- 2.1 (F = 1.17, P < 0.01). With dexamethasone treatment, the percentage decreased significantly to 22.9 +/- 3.0 and 21.4 +/- 3.6, respectively (t = 6.75 and t = 10.1, P < 0.05).

CONCLUSIONS

NF-kappaB activity and percentage of NF-kappaB p65 positive cells are increased significantly, which is associated with pulmonary injury after entrance of amniotic fluid into blood and dexamethasone could inhibit NF-kappaB translocation to the nucleus to degrade NF-kappaB activity and alleviate pulmonary injury. NF-kappaB may be relevant to the occurrence and development of multiple organ dysfunction syndrome.