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Neuroprotective Effect of Ulinastatin on Spinal Cord Ischemia-Reperfusion Injury in Rabbits.

Liu B, Huang W, Xiao X, Xu Y, Ma S, Xia Z - Oxid Med Cell Longev (2015)

Bottom Line: Ulinastatin administration significantly improved postischemic neurologic function with concomitant reduction of apoptotic cell death.In addition, ulinastatin treatment increased SOD activity and decreased MDA content in the spinal cord tissue.These results suggest that ulinastatin significantly attenuates spinal cord ischemia-reperfusion injury and improves postischemic neuronal function and that this protection might be attributable to its antioxidant and antiapoptotic properties.

View Article: PubMed Central - PubMed

Affiliation: Department of Anesthesiology, The 2nd People's Hospital of Guangdong Province, Guangdong Provincial Emergency Hospital, Guangzhou 510317, China.

ABSTRACT
Ulinastatin (UTI), a trypsin inhibitor, is isolated and purified from human urine and has been shown to exert protective effect on myocardial ischemia reperfusion injury in patients. The present study was aimed at investigating the effect of ulinastatin on neurologic functions after spinal cord ischemia reperfusion injury and the underlying mechanism. The spinal cord IR model was achieved by occluding the aorta just caudal to the left renal artery with a bulldog clamp. The drugs were administered immediately after the clamp was removed. The animals were terminated 48 hours after reperfusion. Neuronal function was evaluated with the Tarlov Scoring System. Spinal cord segments between L2 and L5 were harvested for pathological and biochemical analysis. Ulinastatin administration significantly improved postischemic neurologic function with concomitant reduction of apoptotic cell death. In addition, ulinastatin treatment increased SOD activity and decreased MDA content in the spinal cord tissue. Also, ulinastatin treatment suppressed the protein expressions of Bax and caspase-3 but enhanced Bcl-2 protein expression. These results suggest that ulinastatin significantly attenuates spinal cord ischemia-reperfusion injury and improves postischemic neuronal function and that this protection might be attributable to its antioxidant and antiapoptotic properties.

No MeSH data available.


Related in: MedlinePlus

Hind-limb function indicated a progressive decline in function of ischemia-reperfusion IR controls. The scores of Sham group at the same time point were higher than UTI + IR and IR groups (*P < 0.05). The scores of hind-limb function in IR group declined from 4 h to 48 h, but rabbits treated with UTI (UTI + IR group) did not decline; their function stabilized and was significantly greater (#P < 0.01) than that in the IR controls at 24 h and 48 h after reperfusion. In UTI + IR group, function score was higher at 24 h and 48 h time points than at 4 h and 12 h time points (⧫P < 0.05), but the score of IR group was higher at 4 h time point than at the other time points (⧫P < 0.05). Values are the means ± SD, n = 8 per group.
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fig1: Hind-limb function indicated a progressive decline in function of ischemia-reperfusion IR controls. The scores of Sham group at the same time point were higher than UTI + IR and IR groups (*P < 0.05). The scores of hind-limb function in IR group declined from 4 h to 48 h, but rabbits treated with UTI (UTI + IR group) did not decline; their function stabilized and was significantly greater (#P < 0.01) than that in the IR controls at 24 h and 48 h after reperfusion. In UTI + IR group, function score was higher at 24 h and 48 h time points than at 4 h and 12 h time points (⧫P < 0.05), but the score of IR group was higher at 4 h time point than at the other time points (⧫P < 0.05). Values are the means ± SD, n = 8 per group.

Mentions: Hind-limb function was recorded using the Tarlov Scoring System (Figure 1). In the Sham group, the scores from 4 to 48 h after reperfusion did not significantly change (P > 0.05), but in the UTI + IR group the scores were higher at 24 h and 48 h time points than at 4 h and 12 h time points (P < 0.05). The score in the IR group was higher 4 h after reperfusion than 12 to 48 h (P < 0.05). At 24 h and 48 h time points, the hind-limb function of UTI + IR group animals was improved compared to that of IR group animals (P < 0.01), but it did not reach the level of Sham group (P < 0.05).


Neuroprotective Effect of Ulinastatin on Spinal Cord Ischemia-Reperfusion Injury in Rabbits.

Liu B, Huang W, Xiao X, Xu Y, Ma S, Xia Z - Oxid Med Cell Longev (2015)

Hind-limb function indicated a progressive decline in function of ischemia-reperfusion IR controls. The scores of Sham group at the same time point were higher than UTI + IR and IR groups (*P < 0.05). The scores of hind-limb function in IR group declined from 4 h to 48 h, but rabbits treated with UTI (UTI + IR group) did not decline; their function stabilized and was significantly greater (#P < 0.01) than that in the IR controls at 24 h and 48 h after reperfusion. In UTI + IR group, function score was higher at 24 h and 48 h time points than at 4 h and 12 h time points (⧫P < 0.05), but the score of IR group was higher at 4 h time point than at the other time points (⧫P < 0.05). Values are the means ± SD, n = 8 per group.
© Copyright Policy - open-access
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC4487342&req=5

fig1: Hind-limb function indicated a progressive decline in function of ischemia-reperfusion IR controls. The scores of Sham group at the same time point were higher than UTI + IR and IR groups (*P < 0.05). The scores of hind-limb function in IR group declined from 4 h to 48 h, but rabbits treated with UTI (UTI + IR group) did not decline; their function stabilized and was significantly greater (#P < 0.01) than that in the IR controls at 24 h and 48 h after reperfusion. In UTI + IR group, function score was higher at 24 h and 48 h time points than at 4 h and 12 h time points (⧫P < 0.05), but the score of IR group was higher at 4 h time point than at the other time points (⧫P < 0.05). Values are the means ± SD, n = 8 per group.
Mentions: Hind-limb function was recorded using the Tarlov Scoring System (Figure 1). In the Sham group, the scores from 4 to 48 h after reperfusion did not significantly change (P > 0.05), but in the UTI + IR group the scores were higher at 24 h and 48 h time points than at 4 h and 12 h time points (P < 0.05). The score in the IR group was higher 4 h after reperfusion than 12 to 48 h (P < 0.05). At 24 h and 48 h time points, the hind-limb function of UTI + IR group animals was improved compared to that of IR group animals (P < 0.01), but it did not reach the level of Sham group (P < 0.05).

Bottom Line: Ulinastatin administration significantly improved postischemic neurologic function with concomitant reduction of apoptotic cell death.In addition, ulinastatin treatment increased SOD activity and decreased MDA content in the spinal cord tissue.These results suggest that ulinastatin significantly attenuates spinal cord ischemia-reperfusion injury and improves postischemic neuronal function and that this protection might be attributable to its antioxidant and antiapoptotic properties.

View Article: PubMed Central - PubMed

Affiliation: Department of Anesthesiology, The 2nd People's Hospital of Guangdong Province, Guangdong Provincial Emergency Hospital, Guangzhou 510317, China.

ABSTRACT
Ulinastatin (UTI), a trypsin inhibitor, is isolated and purified from human urine and has been shown to exert protective effect on myocardial ischemia reperfusion injury in patients. The present study was aimed at investigating the effect of ulinastatin on neurologic functions after spinal cord ischemia reperfusion injury and the underlying mechanism. The spinal cord IR model was achieved by occluding the aorta just caudal to the left renal artery with a bulldog clamp. The drugs were administered immediately after the clamp was removed. The animals were terminated 48 hours after reperfusion. Neuronal function was evaluated with the Tarlov Scoring System. Spinal cord segments between L2 and L5 were harvested for pathological and biochemical analysis. Ulinastatin administration significantly improved postischemic neurologic function with concomitant reduction of apoptotic cell death. In addition, ulinastatin treatment increased SOD activity and decreased MDA content in the spinal cord tissue. Also, ulinastatin treatment suppressed the protein expressions of Bax and caspase-3 but enhanced Bcl-2 protein expression. These results suggest that ulinastatin significantly attenuates spinal cord ischemia-reperfusion injury and improves postischemic neuronal function and that this protection might be attributable to its antioxidant and antiapoptotic properties.

No MeSH data available.


Related in: MedlinePlus