Study on Endogenous Cannabinoid Receptors CB1 of Brain Injury in Chronic Intermittent Hypoxia Rat Model

SESSION TITLE: Sleep Disorders III SESSION TYPE: Original Investigation Poster PRESENTED ON: Saturday, April 16, 2016 at 11:45 AM - 12:45 PM PURPOSE: By observing the production of calcium/calmodulin dependent protein kinase II (CaMKII) and endogenous cannabinoid system (ECs) receptors CB1 in cerebral hippocampus cells, this study was designed to investigate the effect of CaMKII and CB1 during the course of brain injury of chronic intermittent hypoxia (CIH) with rat model. METHODS: 60 healthy male rats were exposed to the different groups: four weeks (4W) and six weeks (6W) rats of the control groups (CG), 4W and 6W rats of intermittent hypoxia groups (IH), 4W and 6W rats of hypoxic intervention groups (HI) which were intraperitoneal injection with CB1 antagonist (rimonabant) by 1.5mg/kg/d (before modeling). Test animals had been performed after four weeks or six weeks. Morphological changes of brain tissue were observed by hematoxylin-eosin staining (HE). The expression of CaMKII and CB1 receptor in cerebral hippocampus cells were detected by immunohistochemistry detection. RESULTS: 1. HE staining pathological changes in brain cells of rats: the cells in CG neatly arranged was significantly. The brain cells in IH group for four weeks were damaged, cytoplasm sparse, boundaries unclear; while the cells for six weeks were disorganized, density decreased, quantity reduced. Four weeks of brain cells in HI group were neatly arranged basically, cells were relatively clear; as to six weeks cells were swelling, scarce cytoplasm, nuclear stained. 2. Compared with CG, in IH group the expressions of CaMKII and CB1 receptor in cerebral hippocampus were elevated, and with the duration of hypoxia, their expressions were more remarkable. 3. Compared with IH group, the HI group CB1 expression results were lower. 4. Correlation analysis: IH group expression levels of CaMKII and CB1 receptor were positively correlated significantly. CONCLUSIONS: 1. It was confirmed that the unique pathophysiological process of OSAS would indeed lead to ECS disorder; 2. CB1 expression might cause a certain extent of brain damage in CIH; 3. CB1 receptor antagonists (rimonabant) would have a protective effect while the brain occur CIH; 4. CaMKII was activated in the rat brain hippocampus and that might be one of the mechanisms of cognitive impairment. CLINICAL IMPLICATIONS: With the incidence of OSAS are increasing, they cause us more and more attention that brain damage is caused by cognitive disorders and neurological diseases. CB1 expression and effect by OSAS on brain should be gotten to the mechanism, which could help us to discover new drug to improve the quality of life in patients with OSAS. DISCLOSURE: The following authors have nothing to disclose: Xiaoling Gao, Bei Wang, Shujie Wu discussing information about a product/procedure/technique that is considered research.