فهرست مطالب javad raouf sarshoori

We aimed to evaluate whether Liraglutide can remove the deteriorating impact of a high-fat diet (HF) diet on the genitourinary system. Fifty-six C57 mice were recruited of which received an HF as the intervention group, and a chow diet (CH) as a control group. After two months the case group was sub-grouped into three groups; 1: group HF with a daily injection of 0.4mg/kg liraglutide (HF+Lir), 2: CH with a daily injection of 0.4mg/kg liraglutide (CH+Lir), and 3:  HF diet with an infusion of normal saline (HF+NS). After two months, all mice were sacrificed for additional testing. Serological analysis showed no significant difference for lipid profile (P-value>0.05) and hormones except for PSA in males (P-value=0.019). This significance was seen when comparing CH+Lir and HF+NS to the control group (P-values=0.014 and 0.025, respectively). Liraglutide decreases testosterone in both genders and adiponectin and insulin in males. Total sperm count was decreased, and the difference between the groups was significant (P-value=0.013). Liraglutide cannot recover the deteriorating impact of an HF diet on sperm morphology and motility but can improve the sperm DFI and the total number of sperm.

 Cardiovascular diseases are the most important causes of death worldwide. Atherosclerosis, as a common form of cardiovascular disease, tends to involve specific areas of the circulatory system. Boron has anti-inflammatory and antioxidant properties with potential beneficial effects. In this study, we investigated the effect of Boron on histopathological changes of atherosclerotic plaque and lipid profile in hyperlipidemic rabbits.

 Male rabbits in five groups of control, sham, hyperlipidemia, treatment 1 and treatment 2 were fed on high fat diet (1% cholesterol). Treatment groups received Boron, 4 mg / kg, on the first and 20th days of experiment. Animals’ weights were measured on days 1, 21 and 60. Plasma levels of Cholesterol, LDL, HDL and TG were measured by photometric method. After 60 days, Sudan IV staining method was used for macroscopic study. Hematoxylin-eosin and Masson’s trichrome staining method were performed for quantitative analysis.

 Animals in the control and sham groups showed no significant change in serum lipid profile with no atherosclerotic plaque in aortic vessels. In the hyperlipidemia group, significant alterations in lipid profile and presence of atheroma plaques were detected. In animals receiving Boron as a protective agent, atheroma plaques were significantly less (p <0.05). This was confirmed by quantitative analysis.

 Boron ameliorates the development and progression of atherosclerotic plaques. Boron can be used alone or in combination with other drugs as anti-atherosclerotic treatment.

The beneficial outcomes of bone marrow-derived mesenchymal stem cell (BMSC) treatment on functional recovery following stroke has been well established. Furthermore, 5-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors have also been shown to increase neuronal survival and promote the movement of BMSCs towards the sites of inflammation. However, the precise mechanisms mediating the improved neurological functional recovery in stoke models following a combination treatment of Simvastatin and BMSCs still remained poorly understood.
Here, an embolic stroke model was used to experimentally induce a focal ischemic brain injury by inserting a preformed clot into the middle cerebral artery (MCA). Following stroke, animals were treated either with an intraperitoneal injection of Simvastatin, an intravenous injection of 3 ×106 BMSCs, or a combination of these two treatments.
Seven days after ischemia, the combination of Simvastatin and BMSCs led to a significant increase in BMSC relocation, endogenous neurogenesis, arteriogenesis and astrocyte activation while also reducing neuronal damage when compared to BMSC treatment alone (P
These results further demonstrate the synergistic benefits of a combination treatment and help to improve our understanding of the underlying mechanisms mediating this beneficial effect.

Previous findings have shown the crucial roles of brain renin-angiotensin system (RAS) in pathogenesis of Alzheimer’s disease (AD). Since RAS inhibitors may have beneficial effects on dementia and cognitive function in elderly people, the aim of present study was to examine the neuroprotective actions of captopril and valsartan on memory function and neuronal damage in experimental model of AD.
Adult forty male Wistar rats (220-280g) were randomly divided into 5 groups; Control, Vehicle, Alzheimer and treatment groups. AD was induced by the injections of streptozotocin (3mg/kg, bilateral intracerebroventricular) at days 1&3. Treated rats received orally captopril (50mg/kg/day) and valsartan (30mg/kg/day). Memory function and histological assessments were done at termination of experiment. Finally, superoxide dismutase (SOD) and catalase (CAT) activities as well as malondialdehyde (MDA) and NOx contents were determined.
There was a significant increase in the mean value of latency in Alzheimer group (66%). Captopril and valsartan considerably decreased this value in both treatment groups (45% and 72%, respectively). In Alzheimer group the activities of brain’s SOD and CAT reduced (40% and 47%, respectively) in accompany with an increase in MDA and NOx contents (49% and 50%, respectively). Captopril and valsartan significantly increased the activities of brain’s SOD and CAT concomitant reduction in MDA and NOx contents. Also, histopathological damages noticeably decreased in both treatment groups.
Our findings indicate that RAS inhibition by using captopril and valsartan potentiates the antioxidant defense system of brain and reduces oxidative/nitrosative stress in accompany with neuronal damage during AD.

Stroke is the third main cause of mortality and the most important origin of disability in the world. Atorvastatin has been shown to have strong anti-inflammatory and antioxidant effects on various pathological conditions. This study aimed to investigate the possible protective effects of atorvastatin on neuronal injury and damage in an experimental model of focal cerebral ischemia in rats. This experimental study was conducted on 32 male Wistar rats, divided in four groups of eight: the control group, ischemia control group, and ischemia treated with atorvastatin (pre-treatment and post-treatment groups). Cerebral ischemia was determined as 90 minutes of middle cerebral artery occlusion, and 24 hours of reperfusion. Atorvastatin (40 mg/kg) was injected intraperitoneally one hour before ischemia induction, and immediately after the initiation of reperfusion. Moreover, evaluation of motor neuron disorders (NDS index), lesion volumes (TTC dyes) and damage recognition were performed 24 hours after the occlusion of the middle cerebral artery. In this study, the occlusion of middle cerebral artery caused significant lesions in the right hemisphere of the rats in the ischemia control group (483±69 mm3), with NDS of 3.20±0.20. Use of atorvastatin in the pre- and post-treatment ischemia groups significantly reduced lesion volumes to 68% and 54%, respectively (P<0.05). In addition, NDS reduced by 25% in both treatment groups (P<0.05). In histological investigations, atorvastatin significantly decreased the number of damaged neurons and eosinophilia, as well as the demyelination of axons and destruction of nerve tissues in the ischemic areas of the brain. According to the results of this study, atorvastatin could effectively reduce the brain damage caused by ischemia-reperfusion, while preventing neuronal destruction and pathological changes of the brain during ischemia.

Some histopathological alterations take place in the ischemic regions following brain ischemia. Recent studies have demonstrated some neuroprotective roles of crocin in different models of experimental cerebral ischemia. Here, we investigated the probable neuroprotective effects of crocin on the brain infarction and histopathological changes after transient model of focal cerebral ischemia. Experiment was performed in four groups of rats (each group; n=8), sham, control ischemia and ischemia treated rats. Transient focal cerebral ischemia was induced by 80 min middle cerebral artery occlusion (MCAO) followed by 24 hr reperfusion. Crocin, at doses 50 and 80 mg/kg, was injected at the beginning of ischemia (IP injection). Neurologic outcome (Neurological Deficit Score, NDS scale), infarct volume (TTC staining) and histological studies were assessed 24 hr after termination of MCAO. Treatment with crocin, at doses 50 and 80 mg/kg, significantly reduced the cortical infarct volume by 48% and 60%, and also decreased striatal infarct volume by 45% and75%, respectively. Crocin at two different doses significantly improved the NDS of ischemic rats. At histological evaluation, crocin, at dose 80 mg/kg more than 50 mg/kg, decreased the number of eosinophilic (prenecrotic) neurons and reduced the fiber demyelination and axonal damage in ischemic regions. Our findings indicated that crocin effectively reduces brain ischemia-induced injury and improves neurological outcomes. Crocin also is a potent neuroprotective factor that can be able to prevent histopathological alterations following brain ischemia.

Stroke is the third leading cause of death and the most important factor of disability in the world. Recent studies have shown that olive oil has antioxidant effects during cerebral ischemia. The present study investigated the probable protective effects of olive oil on the brain infarction and neurological disability after a transient model of focal cerebral ischemia/reperfusion in rats. In this experimental study, 30 adult male wistar rats whose weight ranged 270-320 g were divided into three equal groups. : sham, control ischemia, and ischemia treated. . Transient focal cerebral ischemia was induced by means of 80 min middle cerebral artery occlusion (MCAO) followed by 24 hours reperfusion. Olive oil(1 ml/kg) was intraperitoneally injected into the cases at the beginning of ischemia. Neurologic outcome (NDS scale), infarct volume (TTC staining) and histological studies were done 24 hours after the end of MCAO. Treatment with olive oil significantly reduced the cortical and striatal infarct volume by 65% and 52%, respectively. Olive oil also decreased the NDS of ischemic rats from 3.4±0.1 to 2.5±0.2 in the treated group. Besides, histological studies showed that olive oil reduced the number of eosinophilic and damage neurons in the ischemic area (P< 0.001). The findings of the current study indicated that olive oil effectively reduced ischemia, helped to the reperfusion of injuries, and improved neurological outcome. Olive oil is also a potent neuroprotective factor that is able to prevent neurodegeneration of transient focal ischemia in the beginning of reperfusion at ischemic areas.