The effects of tissue kallikrein on expressions of bradykinin and its receptors in ischemic brain tissue following cerebral ischemia-reperfusion in rats

Objective To investigate the effects of tissue kallikrein on expressions of bradykinin, bradykinin B1 receptor （B1R） and bradykinin B2 receptor （B2R） in ischemic brain tissue following cerebral ischemia-reperfusion in rats. Methods Fifty-four SD rats were randomly divided into three groups： sham operation, normal saline （NS） （2 ml · kg^-1 · d^-1, for 3 days）, and TK （TK 17 5 × 10 ^- 3 U · kg^- 1· d ^-1, for 3 days） groups （n = 18 in each group）. After three days, the neurological deficit score and the measurement of cerebral infarct volume were performed. The concentration of bradykinin in the ischemic region was detected by the enzyme-linked immunosorbent assay （ELISA）. Reverse transcription-polymerase chain reaction （RT-PCR） and Western blot were used to detect the mRNA and protein expressions of B1R, B2R in ischemic brain tissue, respectively. Results Corniced with the NS group, the neurological deficit （6. 17 ± 1.17 vs. 8. 17 ± 1.33; t =2. 000, P =0. 004） and the cerebral infarct volume （29. 67% ±3.78% vs. 37.50% ± 6. 72% ;t = 0. 078, P = 0. 005） in the TK group were reduced significantly; the concentration of bradykinin in ischemic brain tissue in the TK group was increased significantly （9. 25 ± 1.13 vs. 15.53 ± 1.68, t =6. 283, P =0. 000）; the expression of B2R mRNA was up- regulated significantly （1.21 ±0. 17 vs. 2. 15 ±0. 20; t =0. 943, P =0. 000）, but the up-regulation of the B2R mRNA expression was not obvious （0.51 ±0.05 vs. 0.57 ±0.06; t =0.058, P = 0. 141）; the expression of B2R protein in ischemic brain tissue was up-regulated significantly （1.15 ±0. 16 vs. 1.88 ± 0. 21, t = 0. 737, P = 0. 000）, but the up-regulation of B1R was not obvious （0.50 ± 0. 04 vs. 0. 53 ±0. 05, t = 1. 326, P = 0. 214）. Conclusions TK has protective effect on cerebral ischemia-reperfusion in rats. It may increase the bradykinin concentration in ischemic brain tissue, and up-regulate B2R expression, but it has little effect on B1R expression. It is speculated that B2R may play a major role in TK protecting ischemic brain tissue. Key words: Tissue kallikreins;  Brain ischemia;  Reperfusion injury;  Receptors, bradykinin; Rats