The Effect Of Propofol On Spinal Cord Cell Apoptosis In Rat After Abdominal Aorta Occlusion

Objective To investigate the effect of propofol on expression of NF- κ B and cyclinDl after spinal cord ischemia reperfusion(I/R) in rats and explore its mechanism.Methods 60 Adult Wistar rats weighing 200-250g were anesthetized with chloral hydrate (6ml/kg) and divided randomly into two groups: ① ischmia-reperfusion group(I group) (n=30). abdominal aorta occlusion was induced by placement of a microvascular clamp around the abdominal aorta for 20 min. ②propofol protecting group(P group) (n=30) propofol(100mg/kg)was injected by peritoneal cavity after abdominal aorta occlusion .Neuropathologic methods were used to evaluate the degree of spinal cord injury, the expression levels and distribution of nuclear factor- κ apB(NF-κB)and cyclinDl in spinal cord tissues was determined by immunohistochemical technique. The average optical density (OD) value of NF- κ B protein and cyclinDl in each group were assessed in HIPAS-2000 image analysis system. TdT-mediated dUTP-biotin nick end labelling (TUNEL) method measured apoptotic cells. The relative proportion of apoptotic cells were measured by apoptosis index (AI).Results The histopathology changes in P group were obviously less than those in I group; The levels of NF- κB protein increased gradually in 6h after reperfusion , which reached the peak at 1 days, then lowed at 3 days.However, the level of protein in P group reduced strikingly than that in I group at the same time point (P<0.01). The I group showed some cyclinD1 positive cells at 6 h after reperfusion. At 1 day the number rose sharply, then it formed a peak at 3 days and maintained a relatively high level until 7 days. Compared with I group, the positive cells were significantly reduced in P group (P<0.01). The apopotic cells were observed at few in spinal cord neuron after 6h and 1 day in I group and peaked up to 3 days. This pattern of increased positive cells was maintained up to7 days after reperfusion. For the P group, the apoptosis index (AI) declined very significantily compared with I group at all time points studied. (P<0.01).Conclusions Transient ischemia resulted in a marked activation of NF- κB and cyclinD1. The activation of NF- κB and cyclinD1 was associated with apopotosis of neurons. The results suggest that propofol may inhibit neuronal apopotosis by preventing the activation of NF- κB and cyclinD1.