Aerobic exercise training reduces deep-frying oil-induced apoptosis of hippocampal tissue by reducing oxidative stress in male rats.

Deep-frying oil (DFO) contains high amounts of free radicals, and consuming foods prepared with this method causes damage to nervous tissue due to oxidative stress (OS). Since moderate-intensity aerobic exercise training (AT) reduces OS, the current search investigated the effects of AT on OS, apoptosis, and neurogenesis markers in the hippocampal tissue of DFO-fed rats. Eighteen Wistar male rats (200-280 gr) were randomly allocated to a control group fed with normal food (Con-ND), a control group receiving DFO (Con-DFO), and a group receiving DFO-aerobic exercise (EX-DFO) (n = 6 in each). DFO was gavaged for four weeks, five days a week, with a dose of 2 ml. AT included running on a treadmill for four weeks and five sessions per week (40 min per session). The expression of genes B-cell lymphoma 2 (BCL-2), Protein X associated with Bcl-2 (BAX), Caspase-3 (Casp-3), and Caspase-9 (Casp-9) was measured by PCR method. The ELISA method was used to calculate levels of Superoxide dismutase (SOD) and Catalase (CAT) activity, malondialdehyde (MDA), and Brain-Derived Neurotrophic Factor (BDNF). Also, the expression of the proteins Cannabinoid receptor type 1(CB1), Cannabinoid receptor type2 (CB2), Glial fibrillary acidic protein (GFAP), Neuronal nuclei (NeuN), and DNA fragmentation was evaluated by Immunohistochemical and TUNEL staining. DFO feeding led to a significant increase in apoptotic markers, such as BAX, Casp-3, and Casp-9 gene expression, and DNA fragmentation (p ≤ 0.05) while decreasing BDNF concentration SOD activity (p ≤ 0.05). AT significantly reduced the BAX, Casp-3, Casp-9, MDA, CB1, GFAP, and DNA fragmentation (p ≤ 0.05). In conclusion, AT can reduce the harmful effects of feeding with DFO on the hippocampal tissue.

Combination effect of exercise training and eugenol supplementation on the hippocampus apoptosis induced by chlorpyrifos.

The aim of this study was to investigate the combination effect of exercise training and eugenol supplementation on the hippocampus apoptosis induced by CPF. 64 adult male albino rats were randomly selected and devided into eight groups of eight including: control, exercise (EXE), chlorpyrifos (CPF), Control + Oil (Co + Oil), Control + DMSO (Co + DMSO), chlorpyrifos + eugenol (CPF + Sup), chlorpyrifos + exercise (CPF + Exe) and, chlorpyrifos + exercise + eugenol (CPF + Exe + Eu). Four experimental groups received intraperitoneal injection (5 days a week) of 3.0 mg/kg body weight CPF in DMSO for 6 consecutive weeks. The exercise groups performed aerobic 5 days per week over 4 weeks. Eugenol were administered by gavage. Finally, the animals were sacrificed using CO2 gas (a half of the rats were anesthetized with ketamine and xylazine and then perfused) to evaluate hippocampus histology and parameters. The results of this study showed that CPF injection significantly decreased BDNF, AChE and ATP in CA1 area of the hippocampus (p ˂ 0.05). Also, CA1 apoptosis by tunnel assay, it was found that CPF receiving groups with different dosage, showed a significant increase compared to other groups, which was confirmed by increasing cytochrome C and procaspase-3 in CPF groups (p ˂ 0.05). The result of this study show that 4 weeks of exercise training and eugenol supplementation does not improve the destructive effects of CPF in CA1 area of the hippocampus. As a result, it is recommended that future studies longer periods for treatment with exercise and eugenol supplementation.

Aerobic exercise and eugenol supplementation ameliorated liver injury induced by chlorpyrifos via modulation acetylcholinesterase activation and antioxidant defense.

The primary metabolize of chlorpyrifos (CPF) is in the liver tissue, which it can cause oxidative damage and apoptosis in liver cells. The use of exercise with antioxidant supplements could have a protective effects in the liver tissue especially by improve mitochondria function. The aim of the present study was to investigate the protective effect of aerobic exercise and eugenol (Eu) supplementation on destructive effects of CPF in liver tissue. Sixty-four adult male albino rats were randomly divided into eight groups (eight rats in each group). Four experimental groups received intraperitoneal injection of either 3.0 mg/kg body weight CPF in dimethyl sulfoxide for six consecutive weeks. Aerobic exercise was performed 5 days per week over 4 weeks for exercise groups. Finally, the animals were sacrificed for the histomorphometric analysis and biochemical measurement in the liver tissue. The result of this study show that consumption of CPF alone, caused collagen deposition, increased apoptosis, tumor necrosis factor α, malondialdehyde, and decreased catalase, superoxide dismutase, acetylcholinesterase (AChE) compared to control and exercise groups (healthy groups) in liver tissue (P ˂ .05). Prescription of exercises and Eu supplements in CPF consumer groups, neutralized this destructive effects of CPF. However, concomitant administration of Eu with exercise had better effects on liver tissue (P ˂ .05). It seems that consumption of Eu with aerobic exercise have a protective role in tissue destruction, inflammatory damage by improving antioxidant defense and modulating AChE activity in hepatocytes.

Role or Synergistic Interaction of Adenosine and Vitamin D3 Alongside High-Intensity Interval Training and Isocaloric Moderate Intensity Training on Metabolic Parameters: Protocol for an Experimental Study.

BACKGROUND: Obesity is known as one of the major causes of epidemiologic diseases worldwide; therefore, the introduction of treatment strategies by medical professionals, such as the use of various medicines and exercise programs to reduce fat or prevent obesity, is on the rise. Recently, researchers have shown special interest in assessing the effect of lipolytic adenosine and vitamin D deficiency, as well as the effect of exercise, on decreasing body fat percentage. OBJECTIVE: This study has been designed to examine the effect of adenosine and vitamin D3 injections, in conjunction with high-intensity interval training and isocaloric moderate-intensity training, on the metabolic parameters of obesity induced by a high-fat diet. METHODS: This is an experimental study using 92 Wistar rats. At 6 weeks of age, the rats' weights will be recorded, after which they will have 1 week to adapt to their new environment before being divided into 12 groups. The rats will participate in a 2-stage experimental intervention, including a 13-week fattening diet phase followed by a 12-week exercise training phase consisting of an exercise program and the injection of adenosine and vitamin D3. Groups 1 and 2 will have a normal diet, and the other groups will have a diet of 40% fat, with free access to food and water up to the second half of the second stage of the study (end of the sixth week of training). After termination of the interventions, tissue collection and molecular assessments (blood for biochemical, tissues for gene expression analyses, and anthropometrical indexes) will be performed. RESULTS: The project was initiated in April 2017 and completed in December 2017. Data analysis is under way, and the first results are expected to be submitted for publication in November 2018. CONCLUSIONS: We hypothesize that weight loss-induced molecular changes and upregulation will be observed in line with an increase in lipolysis and beta oxidation in muscle and fat tissue as a result of performing isocaloric training in drug-receiving rats and groups on a high-fat diet. INTERNATIONAL REGISTERED REPORT IDENTIFIER (IRRID): RR1-10.2196/10753.