High-fructose intake-induced dyslipidemia and oxidative stress accompanied by hippocampal dysfunctions in hypertensive but not hypertriacylglycerolemic rats.

A high-fructose intake is metabolically analogous to a high-fat diet. The impact of highfructose intake was investigated in spontaneously hypertensive (SHR) and hypertriacylglycerolemic (HTG) rats to find out the impact of which risk factor of metabolic syndrome - hypertension or hypertriacylglycerolemia - will cause more complications. Rats were fed a standard or a fructose diet (F60) with 60% of added fructose for 5 weeks.

Effect of handling on ATP utilization of cerebral Na,K-ATPase in rats with trimethyltin-induced neurodegeneration.

Previously it was shown that for reduction of anxiety and stress of experimental animals, preventive handling seems to be one of the most effective methods. The present study was oriented on Na,K-ATPase, a key enzyme for maintaining proper concentrations of intracellular sodium and potassium ions. Malfunction of this enzyme has an essential role in the development of neurodegenerative diseases.

The effect of venlafaxine on blood pressure and ECG in rats fed with high-fat-fructose diet.

Metabolic syndrome represents one of the major health, social and economic issues nowadays, and affects more than 25% people worldwide. Being a multifactorial health problem, metabolic syndrome clusters various features, such as obesity, dyslipidemia, hyperglycemia and hypertension. Each of these disturbances represents a risk factor for developing cardiovascular disease.

Natural substance rutin versus standard drug atorvastatin in a treatment of metabolic syndrome-like condition.

Background: Metabolic syndrome is a cluster of metabolic risk factors. The clear causes of its development are not known yet and there is no comprehensive treatment of this disease. There is a trend to use natural substances in the treatment of various diseases, but their effects need to be well explored.

Beneficial effect of 6 weeks lasting handling of adult rats on spatial memory in experimental model of neurodegeneration.

Handling is a form of experience which can result in physiological changes depending on the period of postnatal age when performed. There is a lot of evidence about the positive effect of neonatal handling, but a lack dealing with handling of adult rats. Behavioral changes and memory deficits are present in dementia-like disorders.

Effect of metabolic syndrome on neural plasticity and morphology of the hippocampus: correlations of neurological deficits with physiological status of the rat.

Fat-rich diet (FRD) triggers health complications like hypertension, dyslipidemia, hyperglycemia, insulin resistance and non-alcoholic fatty liver disease, known as the risk factors of metabolic syndrome (MetS), which may result in neurological deficits. The impact of MetS on neuronal functions and brain morphology are poorly understood. We induced MetS-like conditions by exposing hypertriacylglycerolemic (HTG) rats to FRD for eight weeks with the aim to study possible neurological dysfunctions.

Pyridoindole SMe1EC2 as cognition enhancer in ageing-related cognitive decline.

Synthetic pyridoindole-type substances derived from the lead compound stobadine represent promising agents in treatment of a range of pathologies including neurological disorders. The beneficial biological effects were suggested to be likely associated with their capacity to ameliorate oxidative damage. In our study, the effect of supplementation with the derivative of stobadine, SMe1EC2, on ageing-related cognitive decline in rats was investigated.

In vivo magnetic resonance approach to trimethyltin induced neurodegeneration in rats.

Trimethyltin (TMT) is commonly used to induce neurodegeneration in mice and rats; however, only scarce data of in vivo magnetic resonance (MR) spectroscopy and imaging characterizing TMT neurotoxicity are available. Our aim was to assess brain metabolite changes and brain atrophy by in vivo MR in the rat model of neurodegeneration induced by TMT. Adult male Wistar rats exposed to TMT (8mg/kg, i.

Progressive increase of lysosomal enzyme activities in hippocampus associated with reduction of population spike in a rat model of neurodegeneration.

Objectives: Extensive effort has been made to identify early markers of neurodegeneration as late stages have no chance of treatment. Recently, many experimental models have been used to study hallmarks of neuronal injury. One of them is the model of trimethyltin (TMT)-induced damage associated with cognitive decline, thus called a model of Alzheimer-like disease.

In Vitro Metabolomic Approach to Hippocampal Neurodegeneration Induced by Trimethyltin.

Search for indicators of neurodegenerative disorders is a hot topic where much research remains to be done. Our aim was to determine proton nuclear magnetic resonance ((1)H-NMR) spectra of brain metabolites in the trimethyltin (TMT) model of neurodegeneration. Male Wistar rats were subjected to TMT or saline and were sacrificed on day 3 or 24 after administration.

Pyridoindole antioxidant-induced preservation of rat hippocampal pyramidal cell number linked with reduction of oxidative stress yet without influence on cognitive deterioration in Alzheimer-like neurodegeneration.

Background: The idea of antioxidant therapy attenuating Alzheimer disease (AD) neuropathology starts to be attractive. Animal models are often used in these studies. An AD-like model of trimethyltin (TMT)-induced neurodegeneration, targeting the hippocampus, involves neuronal cell death and cognitive impairment.

Effect of antioxidants on functional recovery after in vitro-induced ischemia and long-term potentiation recorded in the pyramidal layer of the CA1 area of rat hippocampus.

Ischemic stroke is one of the leading causes of cognitive impairment. Antioxidants may be beneficial in brain diseases in which oxidative stress can be assumed. The effect of two antioxidants, stobadine and its new derivative coded SMe1EC2, was studied on post-ischemic functional recovery in the hippocampus of young and 18-month-old rats.

Early and late stage of neurodegeneration induced by trimethyltin in hippocampus and cortex of male Wistar rats.

Background: Trimethyltin (TMT), a potent neurotoxicant, elicits neuronal death in the limbic system and causes damage particularly in the hippocampus. Current interest relates to the opportunity to use TMT as an experimental model of neurodegeneration in the study of Alzheimer-like diseases.

Objective: In light of recently found species-specific and strain-specific differences in TMT intoxication, the aim of this study was to characterise the model of TMT-induced neurodegeneration in the brain of Wistar rats during early (days 1-3) and late (days 22-24) stage of neuronal damage.

The new pyridoindole antioxidant SMe1EC2 and its intervention in hypoxia/hypoglycemia-induced impairment of longterm potentiation in rat hippocampus.

Previously, the pyridoindole SMe1EC2 was proved to inhibit lipoperoxidation and carbonylation of proteins in rat brain cortex in the system Fe(2+)/ascorbate and improvement of resistance of the rat hippocampus was reported against ischemic conditions in vitro (hypoxia/hypoglycemia) expressed by the enhanced neuronal response recovery in reoxygenation. The hippocampus fulfils many of the criteria for a neuronal correlate of learning and memory. Recently, an impairment of hippocampal long-term potentiation (LTP) was reported under oxidative stress.

Oxidative stress induced by the Fe/ascorbic acid system or model ischemia in vitro: effect of carvedilol and pyridoindole antioxidant SMe1EC2 in young and adult rat brain tissue.

New effective strategies and new highly effective neuroprotective agents are being searched for the therapy of human stroke and cerebral ischemia. The compound SMe1EC2 is a new derivative of stobadine, with enhanced antioxidant properties compared to the maternal drug. Carvedilol, a non-selective beta-blocker, possesses besides its cardioprotective and vasculoprotective properties also an antioxidant effect.

Maternal treatment of rats with the new pyridoindole antioxidant during pregnacy and lactation resulting in improved offspring hippocampal resistance to ischemia in vitro.

Objective: Damage to the developing brain may be caused by maternal environment, nutritional deficiencies, failure of protective mechanisms, etc. Further, the developing brain may be damaged by intrauterine ischemia or by ischemia in newborns complicated by perinatal asphyxia. There is an effort to find agents with neuroprotective effect on the developing brain.

Effect of the new pyridoindole antioxidant SMe1EC2 on functional deficits and oedema formation in rat hippocampus exposed to ischaemia in vitro.

Objectives: The idea of neuroprotective therapy for ischaemic stroke is based on results from studies on experimental animal models of brain ischaemia demonstrating efficacy of many natural and synthetic agents. Contrary to positive conclusions with antioxidants from animal models, clinical experience failed to find neuroprotectants so efficient in human stroke, infarction, brain trauma, tissue preservation, etc. Thus new highly effective neuroprotective agents need to be discovered.

Effect of transient ischemia on long-term potentiation of synaptic transmission in rat hippocampal slices.

Objectives: Long-term potentiation (LTP) of neuronal activity in the hippocampus is thought to be a substrate for learning and memory. The influence of ischemia (IS) (hypoxia/hypoglycemia) on induction of LTP of synaptic transmission (ST) by high frequency stimulation (HFS) was investigated in rat hippocampal slices.

Methods: Neurons were stimulated via Schäffer collaterals and field excitatory postsynaptic potentials (fEPSP) were recorded extracellularly from the CA1 region.

Effect of the pyridoindole SMe1EC2 and compounds affecting A(1) and A(2A) adenosine receptors in rat hippocampus under ischemia in vitro.

The effect of the newly synthesized pyridoindole antioxidant SMe1EC2 (1 micromol/l) and drugs activating or inhibiting adenosine receptors was tested under ischemia. Synaptic transmission was recorded extracellularly before and under 6-min ischemia and 20-min reoxygenation in rat hippocampal slices in vitro. In untreated slices, ischemia elicited failure of synaptic transmission and excitability expressed by a population spike decay (t(0.