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CJAP ›› 2022, Vol. 38 ›› Issue (6): 803-806.doi: 10.12047/j.cjap.6327.2022.146

• ORIGINAL ARTICLES • Previous Articles     Next Articles

Effects of Bosutinib on cerebral ischemia/reperfusion injury in rats

ZHANG Yi1, WU Chao2, ZHANG Qi3, KONG Yyu4, BIAN Xiao-qian5, WANG Ying5, LI Shu2△   

  1. 1. Graduate School, Wannan Medical College,
    2. Basic Medical School, Wannan Medical College, Wuhu 241000;
    3. Geriatrics,Wuhu Second People's Hospital, Wuhu 241000;
    4. School of Public Health, Wannan Medical College,
    5. Clinical College, Wannan Medical College, Wuhu 241000, China
  • Received:2022-06-14 Revised:2022-11-17 Online:2022-11-28 Published:2023-06-12

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 (P<0.05 or P<0.01). Compared with the MCAO and DMSO groups, the above mentioned indexes of the bosutinib group were all decreased significantly (P<0.05 or P< 0.01). Compared with sham group, the expression levels of SIK2 protein in MCAO and DMSO groups had no significant changes(P> 0.05); compared with the MCAO and DMSO group, the expression level of SIK2 protein in the bosutinib group was decreased significantly (P<0.05). Conclusion: Bosutinib reduces cerebral ischemia-reperfusion-induced injury, and its possible mechanism is related to the decreased expression of SIK2 protein and inflammatory factors.

Key words: Bosutinib, cerebral ischemia-reperfusion injury, SIK2, inflammation

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