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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

The expression of Bax, Bcl-2, and caspase-3 detected by immunohistochemistry. IR injury promoted Bax and caspase-3 expression but suppressed Bcl-2 expression. However, ulinastatin suppressed Bax and caspase-3 expression and promoted Bcl-2 expression.  *Compared with IR group (P < 0.01).  #Compared with Sham group (P < 0.01). Values are the means ± SD, n = 8 per group.
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fig3: The expression of Bax, Bcl-2, and caspase-3 detected by immunohistochemistry. IR injury promoted Bax and caspase-3 expression but suppressed Bcl-2 expression. However, ulinastatin suppressed Bax and caspase-3 expression and promoted Bcl-2 expression.  *Compared with IR group (P < 0.01).  #Compared with Sham group (P < 0.01). Values are the means ± SD, n = 8 per group.

Mentions: As shown in Figure 3, spinal cord ischemia-reperfusion resulted in significant increase of Bax and caspase-3 protein expression and decrease of Bcl-2 protein expression as compared with the Sham group. The number of the positive cells containing Bcl-2 protein expression (brown stain) increased in the UTI + IR group compared to the IR control group. The number of positive cells containing Bax and caspase-3 protein expression (brown stain) decreased in the UTI + IR group compared with the IR group.


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)

The expression of Bax, Bcl-2, and caspase-3 detected by immunohistochemistry. IR injury promoted Bax and caspase-3 expression but suppressed Bcl-2 expression. However, ulinastatin suppressed Bax and caspase-3 expression and promoted Bcl-2 expression.  *Compared with IR group (P < 0.01).  #Compared with Sham group (P < 0.01). Values are the means ± SD, n = 8 per group.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4487342&req=5

fig3: The expression of Bax, Bcl-2, and caspase-3 detected by immunohistochemistry. IR injury promoted Bax and caspase-3 expression but suppressed Bcl-2 expression. However, ulinastatin suppressed Bax and caspase-3 expression and promoted Bcl-2 expression.  *Compared with IR group (P < 0.01).  #Compared with Sham group (P < 0.01). Values are the means ± SD, n = 8 per group.
Mentions: As shown in Figure 3, spinal cord ischemia-reperfusion resulted in significant increase of Bax and caspase-3 protein expression and decrease of Bcl-2 protein expression as compared with the Sham group. The number of the positive cells containing Bcl-2 protein expression (brown stain) increased in the UTI + IR group compared to the IR control group. The number of positive cells containing Bax and caspase-3 protein expression (brown stain) decreased in the UTI + IR group compared with the IR group.

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