ABSTRACT
Background: Overexpression of lectin-like low density lipoprotein [LOX-1] receptor plays an important role in hyperglycemia-induced vascular complications such as atherosclerosis. Based on the beneficial effects of exercise on preventing cardiovascular complications of diabetes, we aimed to examine the protective effects of aerobic exercise on expression of LOX-1 receptor and produc on of free radicals inthe heart of diabetic rats
Methods: Four groups of rats were used: [n=5 per group]: sedentary normal, trained normal, sedentary diabetes and trained diabetes. Diabetes was induced by a single intraperitoneal injec on of streptozotocin [50 mg/kg]. The exercise protocol was consisted of swimming 30 min/day, 5 days/week for eight weeks. Plasma glucose was evaluated at initiation, weeks 4 and 8 of experiment. At the end of experiment, rats were sacrificed and the heart was removed for determination of nitrate, malondialdehyde, and LOX-1 gene expression. In normal non-diabetic rats, the blood glucose level was <150 mg/dl; however, the induction of diabetes resulted in levels more than >400 mg/dl. Gene expression of LOX-1 was increased in the heart of diabetic rats. Exercise reduced the gene expression of this protein in diabetic states without reducing the blood glucose. Finally, swimming exercise decreased the malondialdehyde and nitrate levels in heart tissue both in control and diabetic rats
Conclusion: Swimming exercise reduces heart expression of the LOX-1 receptor in accompany with reduc on of free radicals production. Since these parameters are important in generation of diabetic complications, swimming exercise is a good candidate for reducing these complications
ABSTRACT
Background and Aim: Based on recent studies, atorvastatin has some pleiotropic actions such as anti-inflammatory and anti-oxidant effects independent of lipid lowering effects. Regarding the critical role of oxidative stress and inflammation in inducing diabetic neuropathy, the current study aimed at examining the neuroprotective and anti-oxidative stress effects of atorvastatin at the brain tissues in diabetes experimental models
Materials and Methods: Twenty-four male Wistar rats were randomly divided into 4 equal groups including normal, normal treated, diabetic and diabetic treated. The diabetic group were made diabetic by an intravenous injection of streptozotocin [40mg/kg] and the treated group received 40mg/kg/day atorvastatin for 8 weeks. At the end of the experiment, blood samples from the subjects were derived to measure their blood glucose and urea. Finally, the rats were killed under deep anesthesia and their brains were removed in order to measure malondialdehyde [MDA] and to make histopathological assessment
Results: Uncontrolled hyperglycemia [blood glucose >450 mg/dl] significantly increased blood urea in the diabetic group [130 +/- 10 mg/dl] compared with the normal group [58 +/- 7 mg/dl], [P<0.05]. Also, hyperglycemia increased brain MDA of the diabetic group [8.78 +/- 3.07micromol/mg protein] associated with histopathological damages. Atorvastatin significantly decreased blood urea of the diabetic rats [76 +/- 5 mg/dl] accompanied by histopathological damages. Finally, the content of brain MDA significantly decreased in diabetic rats treated with atorvastatin [0.92 +/- 0.31micromol/mg protein], [P<0.05]
Conclusion: The findings of the present study reveal that atorvastatin is able to prevent hyperglycemia-induced diabetic neuropathy and inhibit brain oxidative stress during diabetes. It is probable that reduction of urea is one of the reasons for atorvastatin prevention of hyperglycemia-induced neuropathy
ABSTRACT
Data shows vanadium protects pancreatic beta cells [BC] from diabetic animals. Whether this effect is direct or through the relief of glucose toxicity is not clear. This study evaluated the potential effect of oral vanadyl sulfate [vanadium] on glycemic status and pancreatic BC of normal and diabetic rats. Rats were divided into five groups of normal and diabetic. Diabetes was induced with streptozocin [40 mg/kg, i.v.]. Normal rats used water [CN] or vanadium [1 mg/ml VOSO4, VTN]. Diabetic rats used water [CD], water plus daily neutral protamine Hagedorn insulin injection [80 U/kg, ITD] or vanadium [VTD]. Blood samples were taken for blood glucose [BG, mg/dL] and insulin [ng/dL] measurements. After two months, the pancreata of sacrificed rats were prepared for islet staining. Pre-treated normal BG was 88 +/- 2, and diabetic BG was 395 +/- 9. The final BG in CD, VTD, and ITD was 509 +/- 22, 138 +/- 14, and 141 +/- 14, respectively. Insulin in VTN [0.75 +/- 0.01] and VTD [0.78 +/- 0.01] was similar, higher than CD [0.51 +/- 0.07] but lower than CN [2.51 +/- 0.02]. VTN islets compared to CN had larger size and denser central core insulin immunoreactivity with plentiful BC. CD and ITD islets were atrophied and had scattered insulin immunoreactivity spots and low BC mass. VTD islets were almost similar to CN. Besides insulin-like activity, vanadium protected pancreatic islet BC, and the relief of glucose toxicity happening with vanadium had a little role in this action
ABSTRACT
Background and Aim: 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
Materials and Methods: 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
Results: 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]
Conclusion: 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
ABSTRACT
It is well known that the development of brain oxidative stress is one of the most serious complications of arterial hypertension that evokes brain tissue damage. The aim of this study was to examine the effects of atorvastatin treatment [20 mg/kg/day], as an antioxidant, to prevent the brain tissue oxidative stress in the hypertensive [HTN] rats. Experiments were performed in four groups of rats [n = 5 each group]: sham, sham-treated, HTN and HTN treated. Rats were made HTN by aortic constriction above the renal arteries. After 30 days, rats were slaughtered under deep anesthesia to remove brain hemispheres. After tissue homogenization, enzyme activities of superoxide dismutase [SOD] and catalase [CAT], as well as glutathione [GSH] content and malondialdehyde [MDA] level were determined by biochemical methods. In HTN rats, arterial blood pressure was increased about 40% and brain enzyme activities of SOD and CAT were significantly decreased compared with sham group. Induction of hypertension significantly decreased GSH content and increased MDA level of brain tissue. Treatment with atorvastatin enhanced the activity of SOD and prevented from GSH decrement during hypertension. Based on the findings of this study, treatment with atorvastatin might have saved the brain tissue of HTN rats from hypertension-induced oxidative stress
Subject(s)
Male , Animals, Laboratory , Pyrroles , Hypertension , Oxidative Stress , Rats, Wistar , Brain , Aortic CoarctationABSTRACT
Nitric oxide synthase [NOS] activity is increased during hypertension and cerebral ischemia. NOS inactivation reduces stroke-induced cerebral injuries, but little is known about its role in blood-brain barrier [BBB] disruption and cerebral edema formation during stroke in acute hypertension. Here, we investigated the role of NOS inhibition in progression of edema formation and BBB disruptions provoked by ischemia/reperfusion injuries in acute hypertensive rats. Rats were made acutely hypertensive by aortic coarctation. After 7 days, the rats were randomly selected for the recording of carotid artery pressure, or regional cerebral blood flow [rCBF] using laser Doppler. Ishcemia induced by 60-min middle cerebral artery occlusion [MCAO], followed by 12-h reperfusion. A single i.p. dose of L-NAME [1 mg/kg] was injected before MCAO. After evaluation of neurological disabilities, rats were slaughtered under deep anesthesia to assess cerebral infarction volume, edema, or BBB disruption. A 75-85% reduction in rCBF was occurred during MCAO which returned to pre-occluded levels during reperfusion. Profound neurological disabilities were evidenced after MCAO alongside with severe cerebral infarctions [628 +/- 98 mm[3]], considerable edema [4.05 +/- 0.52%] and extensive BBB disruptions [Evans blue extravasation, 8.46 +/- 2.03 [microg/g]. L-NAME drastically improved neurological disabilities, diminished cerebral infarction [264 +/- 46 mm[3]], reduced edema [1.49 +/- 0.47%] and BBB disruption [2.93 +/- 0.66 microg/g]. The harmful actions of NOS activity on cerebral microvascular integrity are intensified by ischemia/reperfusion injuries during acute hypertension. NOS inactivation by L-NAME preserved this integrity and diminished cerebral edema