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Blood flow in the the background cerebral ischemia after recanalization may remedy the verge of death of nerve cells can also increase the ischemic cell damage, called reperfusion injury. A variety of reasons caused by cerebral ischemia and reperfusion injury, IL-1 (interleukin-1beta, IL-1 beta)-mediated inflammatory mechanism of more mature. Activation of cysteine ??proteases -1 (caspase-1) is an important reason to cause excessive release of IL-1P. Caspase-1 is an important inflammatory signal transduction substances, it depends on its activation Raw factor. NOD-like receptor 1 (NLRP-1) so that no active caspase-1 activation as an important material of the activity of caspase-1. The purpose of the use of middle cerebral artery cerebral ischemia and reperfusion model by observing the neurological function, infarct volume, inflammation index change, as well as NLRP-1, caspase-1 mRNA and protein expression and inflammatory indices relationship, to explore NLRP-1 and caspase-1 in cerebral ischemia-reperfusion injury in rats, cerebrovascular disease acute phase of treatment, and to find new therapeutic targets to provide experimental basis. Methods 144 clean healthy male SD (Sprague-Dawley) rats, weighing 240-300g were randomly divided into normal control group (n = 18), sham operation group (n = 18) and model group (cerebral ischemia reperfusion group, n = 18). Normal control group without surgery, sham operation group only right common carotid artery ligation model rats caused by middle cerebral artery occlusion (Middle Cerebral Artery Occlusion, MCAO) suture method, open hours after reperfusion, according to reperfusion time point divided into 1h, 3h, 6h, 12h, 24h and 48h subgroup. Six rats in each group brains were taken around the ischemic area of ??brain tissue, observe NLRP-1, caspase-1mRNA and protein expression by RT-PCR and Western-blot method. Six rats with formaldehyde, take perfused brain slices after HE staining, the application Keshavarzian's standard detection of ischemic brain tissue inflammation index. Each group remaining 6 rats were used for the the TTC staining calculation infarction area. All results are mean ± standard deviation (x ± s), the experimental data with SPSS.13 statistical software to analyze the differences between groups in the homogeneity of variance test SNK-q test. Relations between indicators Pearson linear correlation test, test level for alpha = 0.05, P lt; 0.05 was considered statistically significant. Results (1) model the success rate of 79.6%. Animal models of five died from overdose of anesthesia, eight died of a subarachnoid hemorrhage, six died of a brain edema, 15 unexplained deaths, three plug wire, but not observed symptoms of neurological deficit. (2) Compared with the normal control group and sham operation group model rats neurological deficit scores increased (p lt; 0.05), 24-48h peaked at 6h. The infarct volume 6h significant increase (p lt; 0.001) reperfusion 24-48h reached the maximum (p lt; 0.001). (3) sham-operated group and normal control group were not observed inflammation, inflammatory index score of 0, the model group h can be observed infarction and minor inflammatory response, 6h began to increase 24-48h reached a peak (p lt; 0.05). (4) normal control group and sham operation group caspase-1 mRNA have the expression of caspase-1 mRNA expression with the normal control group and sham operation group, model group, ischemic side penumbra 6h after ischemia-reperfusion increased (p lt; 0.001), 24h peaked (p lt; 0.05), 6h, 12h, 24h, 48h group and the normal group and sham operation group differences were statistically significant; normal control group and sham operation group caspase-1 45kd certain expression the model group ischemic side penumbra of caspase-1 45kd expression began to increase at 6h after ischemia-reperfusion (p lt; 0.001), 24h peaked (p lt; 0.001); caspase-1 20kd normal control group, no expression, sham operation group trace expression in the model group began to increase after reperfusion 1h (p lt; 0.001), 24h reach peak (p lt; 0.001). 1-48h at each time point (5) cerebral ischemia and reperfusion after ischemia-reperfusion in NLRP-1 mRNA expression and protein stability, no significant change. The normal control group, sham operation group and model expression between subgroups was no significant difference (P gt; 0.05). (6) Caspase-1 expression changes and inflammation index of change showed a positive related (r = 0.829, p lt; 0.01), protein of NLRP-1 expression changes in the protein of caspase-1 expression changes were being related (r 0.346, p lt; 0.05) NLRP-1 protein expression changes associated with inflammation index no correlation (r = 0.160, p gt; 0.05) Conclusion (1) cerebral ischemia-reperfusion injury may be related to the increase of the expression of caspase-1. (2) NLRP-1 may not be through the expression of the change, but indirectly involved in cerebral ischemia-reperfusion injury.
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