ABSTRACT
The purpose of this study was to evaluate the neuroprotective effect of leptin on a non-human primate model of cerebral ischemia. A total of 39 Guangxi macaques were used to establish the primate cerebral-ischemia model. HE staining was used to evaluated the pathological changes. Moreover, magnetic resonance imaging was used for the detection of embolic area. The measurements of behavior observation and cerebral infarction area were also performed. They all received autologous thrombus operation. Furthermore, western blot and RT-PCR were also used to detect the protein and mRNA expression levels of apoptosis-related factors. Our results showed that leptin could reduce the volume of cerebral infarction by about 35%. Behavioral defects can be significantly improved. In addition, mid-term and long-term behavioral deficiencies had been significantly improved by leptin. Moreover, leptin significantly decreased the expression levels of caspase-3 and Bax, and increased the expression levels of Bcl-2. In conclusion, leptin has neuroprotective effects on cerebral ischemia by effectively reducing the volume of cerebral infarction.
Subject(s)
Brain Ischemia , Neuroprotective Agents , Animals , Neuroprotective Agents/pharmacology , Neuroprotective Agents/metabolism , Leptin , Brain , China , Brain Ischemia/drug therapy , Brain Ischemia/metabolism , Brain Ischemia/pathology , Cerebral Infarction/drug therapy , Cerebral Infarction/metabolism , Cerebral Infarction/pathology , Apoptosis , Primates/metabolism , Caspase 3/genetics , Caspase 3/metabolism , Caspase 3/pharmacologyABSTRACT
OBJECTIVE: To explore the value of CT perfusion in early diagnosis and management of superacute local cerebral infarction in rhesus monkeys. METHOD: Acute local cerebral infarction was induced in the rhesus monkeys during digital subtraction angiography (DSA) by introduction of pale thrombus prepared from autologous blood into the M1 branch of the middle cerebral artery (MCA). Plain CT scan and CT perfusion scanning were performed at different time points before and after DSA operation, and the results were analyzed in conjunction with the pathologic changes. RESULTS: Ischemic lesions were displayed on CT perfusion images, which showed local hypoperfusion, reduced cerebral blood flow and volume, and mean transit time delay in the compromised area. Local hypointense infarct area was identified in plain CT scan 24 h after the DSA operation, and the results were in good agreement with pathological examination during autopsy. CONCLUSION: CT perfusion imaging of the brain can accurately capture the cerebral perfusion deficits in acute ischemic stroke before morphologic changes take place, and therefore provides good means for thrombolytic treatment evaluation of stroke.
