Expression and clinical significance of protein disulfide-isomerase A3 in a rabbit model of spinal cord ischemia/reperfusion injury
10.3969/j.issn.2095-4344.2017.24.013
- VernacularTitle:建立兔脊髓缺血再灌注损伤模型PDIA3的表达变化及临床意义
- Author:
Chunxu LI
;
Shanyong ZHANG
;
Zhiping QI
;
Peng XIA
;
Su PAN
;
Chunfang ZAN
;
Xiaoyu YANG
- From:
Chinese Journal of Tissue Engineering Research
2017;21(24):3845-3850
- CountryChina
- Language:Chinese
-
Abstract:
BACKGROUND:At present, spinal cord ischemia/reperfusion injury is considered as the main reason for secondary paralysis after spinal decompression, and to control the levels of stress-related proteins and excitatory amino acids plays an important role in the treatment of spinal cord ischemia/reperfusion injury. OBJECTIVE:To investigate the expression level of protein disulfide-isomerase A3 (PDIA3) after spinal cord ischemia/reperfusion injury in rabbits. METHODS:Thirty-six New Zealand white rabbits were enrolled, the models of spinal cord ischemia/reperfusion injury were established using Zivin's method, and were then randomized into six groups (n=6 per group). The rabbit abdominal aorta in control group was exposed without vascular occlusion and then the abdominal cavity was closed 30 minutes later. In experimental groups, the abdominal aorta was blocked for 30 minutes, followed by 0, 6, 12, 24 and 48 hours of reperfusion, and then the abdominal cavity was closed. The neurological function was evaluated with a modified Tarlov score. The L3-5lumbar vertebrae were removed, and PDIA3 was screened by two-dimensional fluorescence differential gel electrophoresis combined with mass spectrometry, and then its temporal and spatial changes in the spinal cord were detected by western blot assay and immunohistochemistry. RESULTS AND CONCLUSION:The function of hind limbs was improved in all the experimental groups after spinal cord ischemia/reperfusion injury, and the modified Tarlov scores reached the peak at 24 hours after schemia/reperfusion injury, and decreased slightly at 48 hours. The expression of PDIA3 in the control group showed clear imprinting, which was slightly strengthened at 0 hour, became more strengthened at 6-12 hours, significantly reduced to the minimum level at 24 hours, and returned to the level of 6-12 hours at 48 hours after ischemia/reperfusion. Immunohistochemical results showed that there was visible PDIA3 in the cytoplasm of neurons, and the expression level in the interneurons was significantly higher than that in the motor neurons. These results suggest that upregulated PDIA3 appears in the development and progression of spinal cord ischemia/reperfusion injury, indicating that PDIA3 is closely related to spinal cord ischemia/reperfusion injury, which can be used as a new diagnosis and treatment target.
