Chinese Journal of Tissue Engineering Research ›› 2015, Vol. 19 ›› Issue (49): 7938-7944.doi: 10.3969/j.issn.2095-4344.2015.49.012

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Effects of ischemic postconditioning on related pathways and interleukin 8 expression in rat models of focal cerebral ischemia/reperfusion

Li Zhi-xing1, Lv Jing-lei2, Chen Ping1, Zhao Ren-liang2   

  1. 1Qingdao University Medical College, Qingdao 266000, Shandong Province, China; 2Department of Neurology, the Affiliated Hospital of Qingdao University, Qingdao 266003, Shandong Province, China
  • Received:2015-09-07 Online:2015-11-30 Published:2015-11-30
  • Contact: Zhao Ren-liang, M.D., Chief physician, Professor, Master's supervisor, Department of Neurology, the Affiliated Hospital of Qingdao University, Qingdao 266003, Shandong Province, China
  • About author:Li Zhi-xing, Studying for master’s degree, Qingdao University Medical College, Qingdao 266000, Shandong Province, China
  • Supported by:

    a grant from Qingdao Municipal Science and Technology Bureau, China, No. 14-2-3-14-nsh

Abstract:

BACKGROUND: Ischemic postconditioning may motivate endogenous protective effect and inhibit inflammatory response after ischemia/reperfusion, but the specific mechanism is still unclear.
OBJECTIVE: To investigate the effects of ischemic postconditioning on Toll-like receptor 4/nuclear factor кB signaling transduction pathway and interleukin 8 expression in rat models of focal cerebral ischemia/reperfusion, and further illustrate the neuroprotective mechanism of ischemic postconditioning.
METHODS: One hundred and ten rats were randomly divided into sham group (n=10), model group (n=50) and ischemic postconditioning group (n=50). Focal cerebral ischemia/reperfusion rat models were established according to Zea-Longa method, and then subjected to ischemic postconditioning, i.e., middle cerebral artery occlusion for 2 hours followed by 3 cycles of 15-second reperfusion/15-second ischemia. Model group and sham group were set for comparison. In each group, rat neurobehavioral deficit scores were evaluated, and rat infarct volume was measured with TTC staining. The expression of Toll-like receptor 4, nuclear factor кB and interleukin 8 protein in brain tissue was detected by immunohistochemistry. Their mRNA expression was detected 
by in situ hybridization.
RESULTS AND CONCLUSION: Rats in the model and ischemic postconditioning groups all presented neurobehavioral deficits and cerebral hemisphere infarction on the ischemic side. At 6, 12, 24, 48 and 72 hours after reperfusion, the neurobehavioral deficit scores were significantly decreased in the ischemic postconditioning group compared with that in the model group (P < 0.05). The infarct volume of rats in the ischemic postconditioning group was significantly decreased compared with that in the model group (P < 0.05). The expression of Toll-like receptor 4, nuclear factor кB and interleukin 8 protein and mRNA was increased at 6 hours after reperfusion and reached the peak at 24 hours after reperfusion. At 6, 12, 24, 48 and 72 hours after reperfusion, the expression of Toll-like receptor 4, nuclear factor кB and interleukin 8 protein and mRNA was all significantly decreased in the ischemic postconditioning group compared with that in the model group (P < 0.05). The results confirm that ischemic postconditioning may inhibit inflammatory response induced by ischemia/reperfusion, and play its neuroprotective effect by inhibiting Toll-like receptor 4/nuclear factor кB signaling transduction pathway and down-regulating the expression of interleukin-8. 

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