ABSTRACT
Objective: To investigate the effects of bosutinib on the early stage of cerebral ischemia-reperfusion injury in rats. Methods: Forty Sprague-Dawley rats were randomly divided into four groups (random number method), 10 rats in each group; sham group (control group): only neck vessels were isolated without other treatments; MCAO (model group): the rat brain ischemia/reperfusion injury model was made by a modified wire bolus method,ischemia for 2 h followed by reperfusion for 24 h; DMSO group (solvent group): DMSO ( 0.752 ml/kg) was injected into the tail vein one day before the experiment, brain ischemia 2 h reperfusion for 24 h; Bosutinib group (intervention group): one day before the experiment, the tail vein was injected with Bosutinib (4 mg/kg), brain ischemia 2 h reperfusion for 24 h. After 24 h of ischemia reperfusion, neurological function score was performed; brain infarct area was calculated after staining with TTC; SIK2 was detected by Western blot; the contents of TNF-α and IL-6 in brain tissue were detected by ELISA. Results: Compared with the sham group, the neurological function scores, the infarct volume percentages and the levels of inflammatory factors IL-6 and TNF-α of the MCAO and DMSO groups were increased significantly (Pï¼0.05 or Pï¼0.01). Compared with the MCAO and DMSO groups, the above mentioned indexes of the bosutinib group were all decreased significantly (Pï¼0.05 or Pï¼ 0.01). Compared with sham group, the expression levels of SIK2 protein in MCAO and DMSO groups had no significant changes(Pï¼ 0.05); compared with the MCAO and DMSO group, the expression level of SIK2 protein in the bosutinib group was decreased significantly (Pï¼0.05). Conclusion: Bosutinib reduces cerebral ischemia-reperfusion-induced injury, and its possible mechanism is related to the decreased expression of SIK2 protein and inflammatory factors.
