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Objective: The aim of the present study was to assess olive leaf extract (OLE) effects on learning and memory deficits in a model of diabetes induced by streptozotocin (STZ) in rats. Materials and Methods: The rats were divided as: (1) control rats, (2) diabetic rats, and (3-6) diabetic rats treated by 100, 200, and 400 mg/kg of OLE or metformin. Using the passive avoidance test (PA), we investigated fear learning and memory behaviors. In cortical and hippocampus tissues, total levels of malondialdehyde (MDA) and thiol were measured along with the activity of catalase (CAT) and superoxide dismutase (SOD). Results: Learning and memory behavior impairment were significantly developed in diabetic rats as shown by the impairment of the PA task compared to the control group (p<0.001). In addition, elevated levels of MDA and reduced overall concentrations of thiol, CAT and SOD activity were obvious in diabetic rats' cortex and hippocampus tissues (p<0.01-p<0.001). Meanwhile, OLE in a dose-dependent manner, improved memory deficit and cognitive performance that was attributed to a reduction of lipid peroxidation and elevation of total thiol concentration, and CAT and SOD activity levels in the brain tissues (p<0.05-p<0.001). Conclusion: OLE could be effective in improving cognitive impairment in STZ-induced diabetes by oxidative stress depression. [ABSTRACT FROM AUTHOR]

The effect of levothyroxine (L-T4) on the learning and memory impairment induced by streptozotocin (STZ) and brain tissue oxidative damage in rats was evaluated. An animal model of the Alzheimer's disease (AD) was established by intracerebroventricular injection of STZ (3 mg/kg) in male Wistar rats (250 ± 50 g). After that, the rats were treated for 3 weeks with L-T4 (10, 100 μg/kg) or normal saline. Passive avoidance (PA) learning and spatial memory were evaluated using shuttle box and Morris water maze (MWM), respectively. Finally, the rats were euthanized, their blood samples were collected for further thyroxine assessment and their brains were removed after decapitation in order to measure the oxidative stress parameters and brain-derived neurotrophic factor (BDNF). In the MWM, latency (s) increased in the AD rats compared with the normal control group while it decreased in the 10 μg/kg L-T4 injected AD rats compared with the AD group. In the PA, the latency for entering the dark compartment was lower in the AD group than in the normal control group and it decreased in the 10 μg/kg L-T4 injected AD rats. The low dose of L-T4 (10 μg/kg) reduced malondialdehyde concentration but increased thiols concentration, superoxide dismutase, catalase activities and BDNF level in hippocampal tissues of the AD rats. Injection of L-T4 (10 μg/kg) alleviated memory deficits and also improved factors of oxidative stress and BDNF level in the STZ-induced AD rats. [ABSTRACT FROM AUTHOR]

Introduction: Angiotensin converting enzyme (ACE) inhibitors are suggested to have some beneficial effects on the brain. In the present study the protective effects against brain tissues oxidative damage as possible mechanism for learning and memory improving effects of captopril was investigated in scopolamine treated rats. Methods: Fifty male Wistar rats were divided into seven groups and treated: saline as a control group, Sco (scopolamine) and Sco-Capto10, 50 and 100 (captopril 10, 50 and 100mg/kg before scopolamine). Treatment was passive avoidance test and then the cortical tissues were collected to measure malondialdehyde (MDA), nitric oxide (NO) metabolites, thiol, super oxide dismutase (SOD) and catalase (CAT). Results: Scopolamine decreased the latency to enter the dark in passive avoidance test compared to control group. It also increased MDA and NO metabolites while decreased thiol, SOD and CAT in comparison with control group. Captopril increased the latency to enter the dark. It also decreased MDA and NO metabolites while, increased thiol, SOD and CAT. Conclusion: Captopril protected brain tissues oxidative damage and improved learning and memory impairment induced by scopolamine. [ABSTRACT FROM AUTHOR]

Ischaemic heart diseases (IHD) are among the major causes of mortality in the elderly population. Although timely reperfusion is a common treatment for IHD, it causes additional damage to the ischaemic myocardium known as ischaemia-reperfusion (IR) injury. Considering the importance of preventing reperfusion injuries, we aimed to examine the combination effect of mitochondrial transplantation (MT) and coenzyme Q 10 (CoQ 10 ) in myocardial IR injury of aged male rats. Seventy-two aged male Wistar rats were randomly divided into six groups: Sham, IR, CoQ 10 , MT, combination therapy (MT + CoQ 10 ) and vehicle. Myocardial IR injury was established by occlusion of the left anterior descending coronary artery followed by reopening. Young male Wistar rats were used as mitochondria donors. Isolated mitochondria were injected intraventricularly (500 µL of a respiration buffer containing 6 × 10 6 ± 5 × 10 5  mitochondria/mL) in MT-receiving groups at the onset of reperfusion. CoQ 10  (10 mg/kg/day) was injected intraperitoneally for 2 weeks before IR induction. Twenty-four hours after reperfusion, haemodynamic parameters, myocardial infarct size (IS), lactate dehydrogenase (LDH) release and cardiac mitochondrial function (mitochondrial reactive oxygen species (ROS) generation and membrane potential) were measured. The combination of MT and CoQ 10  improved haemodynamic index changes and reduced IS and LDH release (P < 0.05). It also decreased mitochondrial ROS generation and increased membrane potential (P < 0.05). CoQ 10 also showed a significant cardioprotective effect. Combination therapy displayed greater cardioprotective effects than single treatments. This study revealed that MT and CoQ 10 combination treatment can be considered as a promising cardioprotective strategy to reduce myocardial IR injury in ageing, in part by restoring mitochondrial function., (© 2024 The Authors. Experimental Physiology published by John Wiley & Sons Ltd on behalf of The Physiological Society.)