Ischemic postconditioning alleviates cerebral ischemia-reperfusion injury in rats by upregulating brain-derived neurotrophic factor and tyrosine receptor kinase B / 国际脑血管病杂志

ABSTRACT

ObjectiveToinvestigatetherolesofbrain-derivedneurotrophicfactor(BDNF)and tyrosine receptor kinase B (TrkB) in ischemic postconditioning. Methods Wistar rats w ere randomly assigned to three groupsa sham operation (9 rats), an ischemic postconditioning, and an ischemia-reperfusion group. According to the reperfusion time, the latter 2 groups w ere redivided into 6, 12, 24, 48, and 72 h subgroups (9 rats in each subgroups). A middle cerebral artery occluded by suture method for a cerebral ischemia-reperfusion model. Triphenyl tetrazolium staining w as used to detect infarct volume (P=4). Immunohisto-chemical staining w as used to detect the expression levels of BDNF and TrkB proteins (P=5). Results The infarct volumes in the ischemic postconditioning group w ere reduced significantly compared w ith those in the ischemia-reperfusion group (6 h143.3 ±8.7 mm3 vs.166.8 ±7.5 mm3, t=4.104, P=0.006;12 h151.7 ±7.8 mm3 vs.171.6 ±9.1 mm3, t=3.314, P=0.016; 24 h 159.2 ±9.3 mm3 vs.177.1 ± 7.6 mm3, t=3.000, P=0.024;48 h166.9 ±9.6 mm3 vs.184.9 ±9.0 mm3, t=2.732, P=0.034;72 h172.0 ±9.1 mm3 vs.198.1 ±8.2 mm3, t=2.640, P=0.039), and the positive cel numbers of BDNF (6 h23.98 ±4.07 vs.18.63 ±2.5, t=2.479, P=0.038;12 h27.64 ±3.18 vs.22.01 ±3.14, t=2.817, P=0.023;24 h34.82 ±4.17 vs.28.46 ±4.05, t=2.446, P=0.040; 48 h34.30 ±3.27 vs.26.29 ± 3.26, t=3.872, P=0.005;72 h28.77 ±3.53 vs.23.64 ±3.54, t=2.297, P=0.051) and TrkB (6 h33.83 ±3.90 vs.21.51 ±3.86, t=5.012, P<0.001; 12 h38.59 ±4.84 vs.23.41 ±3.67, t=5.586, P<0.001;24 h46.07 ±3.06 vs.28.78 ±3.61, t=8.169, P<0.001; 48 h47.90 ±3.30 vs.29.51 ± 3.81, t=8.160, P<0.001; 72 h42.78 ±4.07 vs.27.46 ±3.19, t=6.623, P<0.001) per high-pow er field at each time point in the ischemic postconditioning group w ere significantly more than those in the ischemia-reperfusion group. Conclusions Ischemic postconditioning upregulates the expressions levels of BDNF and TrkB proteins after ischemia-reperfusion and reduces cerebral infarct volumes. BDNF/TrkB may play an important neuroprotective effect in ischemic postconditioning.