Ischemic tolerance can protect the BRAIN against cerebral ISCHEMIA and neurodegenerative diseases. However, several studies demonstrate ischemic tolerance by various methods, the exact mechanisms of ischemic tolerance has not been clearly understood.In this study, we first studied BRAIN ISCHEMIA-related mechanisms and then evaluated the outcomes of mitochondrial pathophysiology of ischemic tolerance in focal and full stroke animal models.In this study, mitochondrial and peroxisomal reactions are considered critical in ischemic tolerance. In rats and Syrian mice, the middle cerebral artery occlusion (MCAO) model was employed to represent cerebrovascular stroke. Ischemic tolerance exhibits different types of adaptation responses associated with a number of sub-cellular changes.Changes in the cellular non-genomic pathways are usually short and reversible; while, the consequences of genes expression are a long-term process and can lead to permanent alternations in the genes expression pattern. The ischemic tolerance can be clinically significant. Therefore, it is important to address the risks and advantages of ischemic tolerance in non-infarcted tissues such as transplanted ones.

Background: BRAIN ischemic disorders are common diseases of neural systems. One of the predisposing factors affect to the BRAIN ISCHEMIA is systemic hypertension. The aim of this study was the determination of relation between blood pressure and spread of BRAIN ISCHEMIA in CT scan in BRAIN ISCHEMIA patients. Materials & Methods: In the first stage and on the basis of research group, we selected 33 males and 33 females at the age of 45 and more with the diagnosis of BRAIN ISCHEMIA by chance. Then we collected the information of those patients about general information, post history of hypertension and cardiovascular diseases. Then, we recorded degree of systolic and diastolic blood pressure on the first day of bedridden time and recorded specifications of ISCHEMIA in: CT Scan about numbers and extent of ISCHEMIA. In the final stage, we considered relations between systolic and diastolic pressures and extension of ISCHEMIA. Datas were analyzed by EPI6 software. Results: Those finding showed that about 63.3% of patients were in 65 to 74 years old. In 81.8% of them hypertension history was positive. It is also specified that 36.3% of patients had normal systolic blood pressure and 45.4% had normal diastolic blood hypertension, and 63.7% had several ISCHEMIA. The severity .ISCHEMIA in 54 cases (81.8%) were above 2 cm2. It is specified that there was no significant relation between systolic blood pressure and extension of ISCHEMIA in CT scan, but there was a significant relation between diastolic blood pressure and extension of ISCHEMIA (P=0.03). Having the negative history of hypertension in conformity of two indexes was significant (0.03%). There is no significant relation about sex, but there was a significant relation between two indexes and age above 75 years old (P=0.04).Conclusion: It is demonstrated that blood pressure and hypertension without history have a major role in extension of ISCHEMIA and aged is important factor between relation of two indexes.

Background: In patients affected with stroke, most ischemic episodes (80-90%) occur due to occlusion of middle cerebral artery (MCA).Methods: Some of blood through femoral artery was withdrawn into a PE- 50 catheter and kept for 2 h in room temperature and 22 h at 4oC to allow old clot formation. Then the catheter was advanced 17 mm in the internal carotid artery until its tip was 1 to 2 mm away from MCA origin. 3-5ml the preformed clot or 5ml saline (for sham- operated animals) were injected. Behavioral deficits and seizure activities were recorded at 2, 24, and 48 hours after clot injection. Then the rats were decapitated to remove the BRAINs and prepare them for Tetrazoliume chloride (TTC) staining and analyzing.Findings: When 3 or 5 Yl clots were injected, infarct volume was 29.35±1.26% and 16.15±94% respectively (p<0.05). BRAIN edema also was 8.6±1.65% and 3±1.74%, respectively (p<0.05). There was a significant correlation between infarct volume and BRAIN edema (r=0.56, p<0.05). Behavioral deficit score at 48 hours after clot injection between two groups were significantly different (p<0.05).Conclusion: This model is very similar to thromboembolic stroke in human and prepares a reliable method for investigating the stroke mechanism. It would also be useful for studying thromboembolic agents effect on stroke and BRAIN ischemic injury.

BACKGROUND AND OBJECTIVE: The use of antioxidants has been considered for the prevention and treatment of ischemic complications, particularly in the BRAIN. Previous study showed a reduction in cell death in BRAIN ISCHEMIA before and after treatment with antioxidants. The aim of this study was to investigate the effect of olive oil on Temporal cortical cell death following ISCHEMIA reperfusion injury.METHODS: This study was performed on 21 adult male BALB/c mice (35-40 g). Experimental design includes three groups: intact group (n=7), ischemic control (n=7), treatment groups with olive oil (n=7). The mice treated with olive oil (180 micro liter) as pre- treatment for a week. Then, ISCHEMIA in temporal cortex lob induced by common carotid artery occlusion (for 15 minutes) and following the reduction in inflammation (a week), the mice post-treated with olive oil. Nissl staining applied to counting necrotic cells and Tunnel kit was used to quantify apoptotic cell death in temporal cortex lob.FINDINGS: There was a significant increase in cell death in temporal cortex lob in ischemic samples in compared to control group (30-35 cells increased in treatment group compared to ISCHEMIA group) (p<0.05). There was a significant decrease in cell death rate in treatment group in compared to ISCHEMIA group (50-55 cells decreased in ISCHEMIA group compared to control group) (p<0.05).CONCLUSION: Our findings showed that olive oil consumption significantly reduced cell death following ISCHEMIA reperfusion injury.

Background and Aim: Increasing evidence has demonstrated that activation of peroxisome proliferator-activated receptor alpha (PPARα ), which belongs to the nuclear receptor family of ligand-activated transcription factors, after cerebral ISCHEMIA exhibit neuroprotective functions including anti-oxidative, anti-apoptotic and anti-inflammatory effects. The aim of this study was to evaluate the pretreatment effects of PPARα agonist, fenofibrate, on BRAIN infarction, tissue swelling and BRAIN edema in an experimental model of ischemic stroke. Materials and Methods: The study included three groups of rats (N=36); sham, control ischemic and treated ischemic groups. BRAIN ISCHEMIA was induced by 90 min middle cerebral artery occlusion (MCAO) followed by 24 hours reperfusion. Rats received fenofibrate (200 mg/kg/day) by oral route for 4 days before induction of MCAO. Neurological deficit score (NDS), infarct volume (TTC staining method), tissue swelling and BRAIN edema were assessed 24 hours after termination of MCAO. Results: MCAO induced neurological dysfunction (2. 83± 0. 16), BRAIN infarction (282± 30 mm3), BRAIN swelling (15. 13± 2. 29 %) and edema (17. 23± 1. 97%) in control ischemic group. Administration of fenofibrate in the treated ischemic rats significantly reduced neurological dysfunction (2. 14± 0. 14), BRAIN infarction (92± 28 mm3), BRAIN swelling (4. 35± 1. 42%) and edema (5. 49± 1. 44) compared to the rats in the control ischemic group. Conclusion: Our findings indicated that activation of PPARα by specific agonist, fenofibrate, effectively decreased the cerebral ISCHEMIA-reperfusion injuries as well as BRAIN swelling and edema in an experimental model of ischemic stroke.