ABSTRACT
Glucagon-like peptide 1(GLP-1) is an important member of incretin.Takingitoralymay stimulate the terminal ileum and colon L cel s to secrete GLP-1. After GLP-1 biding specific receptor GLP-1 receptor ( GLP-1R), it exerts the roles of promoting glucose-dependent insulin secretion, inhibiting glucagon secretion, and decreasing plasma glucagon level. The molecular mass of GLP-1 is relatively smal er and can directly cross the blood-brain barrier, and both central and peripheral nervous systems have the GLP-1R expression. GLP-1 significantly improves neurological deficits and reduces infarct volume. It may exert neuroprotective effect through the mechanisms of inhibiting the inflammatory response, oxidative stress, and cel apoptosis. This article review s the discovery of GLP-1, its biological characteristics and neuroprotective effect in cerebral ischemia.
ABSTRACT
Objective To investigate the relationship between the matrix metalloproteinase-3(MMP-3)and the stability of carotid artery plaque,and explore MMP-3's prediction role on the attack and relapse of acute ischemic cerebrovascular events.Methods 100 patients with the first ever acute cerebral infarction,100 patients with chronic cerebral circulation insufficiency(CCCI)and 40 persons without cerebrovascular diseases were enrolled in this study.According to the carotid ultrasound examination,100 cerebral infarction patients were divided into three subgroup: unstable plaque group(45 patients,mixed plaque,soft plaque),stable plaque group(35 patients,plaque Group)and endometrial coarse group(25patients).Matrix metalloproteinase-3(MMP-3)levels of all the subjects were measured by enzyme-linked immunosorbent assay(as basal level).All the subjects were followed up for one year to observe cerebral infarction events.Serum MMP-3 levels of each group,and the basic serum MMP-3 levels were compared among patients who were attacked or relapsed cerebral ischemic with those who had not been attack cerebral ischemic during this period of time.Results 5 patients in the cerebral infarction group had relapse (5%),2 patients in the CCCI group were attacked by cerebral ischemic(2%),and no one in the normal control group was attacked by cerebral ischemic.Serum MMP-3 levels in the acute cerebral infarction group were significantly higher than CCCI group,and both groups were significantly higher than normal control group (P ＜0.05).The basic serum MMP-3 levels in all patients who were attacked by cerebral ischemic were significantly higher than those who had not been attack by cerebral ischemic during this period of time(P ＜0.05).The serum MMP-3 levels of the unstable plaque group were significantly higher than stable plaque group.And both groups were significantly higher than endometrial coarse group(P ＜0.05).Conclusions Elevated levels of matrix metalloproteinase-3(MMP-3)might have something with the stability of carotid atherosclerotic plaque,and participate the attack and the relapse of acute cerebral infarction.Determination of MMP-3 might be used to predict the attack and relapse of acute cerebral infarction.
ABSTRACT
One hundred patients with acute ischemic stroke were enrolled in the study as the trial group, and 20 healthy individuals as control group. Intima-media thickness and plaque of the carotis were detected by carotid ultrasonography, cerebral infarction was detected by CT/MRI, and serum concentrations of sCD40L were measured by enzyme-linked immunosorbent assay. Neurologie impairment score was evaluated in all patients. The results showed that in patients with acute ischemic stroke the serum concentrations of sCD40L in plaques group were significantly higher than those in no plaque group. The levels of serum sCD40L of infarction group (diameter>1.5 cm) were higher than those of lacunar infarction group ( diameter<1.5 cm ) and temporary ischemic attack ( TIA ) group. The levels of serum sD40L in trial group were all higher than those in control group. In the trial group, serum concentrations of sCD40L were correlated with neurologic impairment score. The results indicate that CD40/CD40L signaling pathway may be involved in the carotid atherosclerosis formation and the rupture of plaques, and the increase of serum CD40L levels might be a risk factor for acute ischemic cerebrovascular diseases.