부산대학교 도서관

Changes in visfatin, as an adipocytokine, after cerebral infarction with diabetes and its pathophysiological significance are not clear. We attempted to elucidate the relationship between changes in visfatin after cerebral infarction with diabetes and pathogenesis. Protein levels of visfatin in brain tissue after middle cerebral artery occlusion/reperfusion (MCAO/R) in db/db mice did not change compared with those of the non-diabetic and control groups, but they were significantly increased in the cerebrovascular fraction. This increase would be derived from astrocytes as a monomer, which is involved in inflammation, around the cerebral blood vessels. The increase in MMP-9 mRNA of the cerebrovascular fraction might be due to the increased monomeric form of visfatin. Interestingly, there were no changes in visfatin mRNA in the cerebrovascular fraction, while protein levels of dimeric form of visfatin, which contributes to neuroprotection, were increased in serum after MCAO/R with diabetes. Therefore, visfatin could be secreted into the blood from peripheral tissues as a dimer after MCAO/R with diabetes, and a part of it changes into a monomer in the process of infiltration into the brain parenchyma. Monomeric forms of visfatin may be involved in an inflammatory reaction and the pathogenesis of cerebral infarction with diabetes.