Voluntary wheel running from early adolescence reduces disease progression, and anxiety- and depression-related symptoms in an adult male mouse model of rheumatoid arthritis.

Rheumatoid arthritis (RA) is a multifactorial autoimmune disease that progressively destroys synovial joints and leads to chronic systemic inflammation. This autoimmune disorder is associated with increased anxiety- and depression-related symptoms, which reduces quality of life. Clinical and experimental evidence suggests that higher physical activity from early adolescence may prevent chronic diseases and reduce the risk of mental health problems in adulthood. This study aimed to assess whether voluntary wheel running from early adolescence can decrease clinical symptoms, anxiety- and depression-related behaviors in adult mice with rheumatoid arthritis. Adolescent male mice were exposed to voluntary wheel running until adulthood and got collagen-induced arthritis. We measured body weight, the thickness of the hind paw and knee joint (clinical signs), anxiety- and depression-related behaviors, serum testosterone, and cytokines (IFN-γ IL-1ß, IL-6, TNF-α, IL-10). The findings showed that collagen-induced arthritis resulted in anxious-like behavior, increased anhedonia, elevated IL-6, IL-1ß, TNF-α, and IFN-γ, and decreased testosterone levels in the serum of mice. However, no change was observed in behavioral despair. We found that higher physical activity from early adolescence significantly reduced the severity of clinical signs, anxiety- and anhedonia-like behaviors, and decreased behavioral despair in RA-induced mice. In addition, the running wheel exposure normalized RA-induced abnormalities in testosterone and inflammatory cytokines in mice. Altogether, this study suggests that higher physical activity from early adolescence may make mice less vulnerable or resistant to RA-induced clinical symptoms and anxiety- and depression-related behaviors by changing testosterone and inflammatory cytokines productions in adulthood.

Fluoxetine combined with swimming exercise synergistically reduces lipopolysaccharide-induced depressive-like behavior by normalizing the HPA axis and brain inflammation in mice.

Major depression disorder is a debilitating psychiatric disease affecting millions of people worldwide. This disorder is the leading cause of morbidity and mortality in high-income countries. Selective serotonin reuptake inhibitors such as fluoxetine are first-line drugs for treating depression-related disorders, but not all patients respond well to these antidepressants. This study aimed to evaluate whether fluoxetine combined with aerobic exercise can affect lipopolysaccharide (LPS)-induced depressive-like behavior, hypothalamic-pituitary-adrenal (HPA) axis dysregulation, and brain inflammation in mice. Male mice were exposed to fluoxetine, swimming exercise, or a combination of both and finally treated with LPS. We measured depression-related symptoms such as anhedonia, behavioral despair, weight gain, and food intake. Hormones (corticosterone and testosterone) and cytokines (IL-1ß, IL-6, TNF-α, IL-10) were also measured in serum and brain (hippocampus and prefrontal cortex), respectively. The findings indicated that LPS induced anhedonia and behavioral despair and increased corticosterone, hippocampal IL-1ß, TNF-α, and decreased testosterone and hippocampal IL-10 in mice. Fluoxetine and exercise separately reduced LPS-induced depressive-like behavior, while their combination synergistically reduced these symptoms in LPS-treated mice. We found fluoxetine alone increased food intake and body weight in LPS-treated mice. Fluoxetine and exercise combination reduced corticosterone, hippocampal TNF-α, and prefrontal IL-6 and TNF-α levels and increased testosterone and hippocampal and prefrontal IL-10 levels more effectively than fluoxetine alone in LPS-treated mice. This study suggests that swimming exercise combined with fluoxetine can affect depression-related behavior, HPA axis, and brain inflammation more effectively than when they are used separately.

Physical activity in a swimming pool attenuates memory impairment by reducing glutamate and inflammatory cytokines and increasing BDNF in the brain of mice with type 2 diabetes.

Type 2 diabetes is a risk factor for the development of cognitive impairment. Increasing evidence suggests that regular exercise is beneficial for the treatment of clinical symptoms in diabetic patients. The current study aimed to evaluate whether increasing physical activity through swimming training can reduce memory impairment in an animal model of type 2 diabetes. Diabetes and non-diabetes mice underwent swimming training for four weeks, and then working, spatial, and recognition memory were evaluated using three behavioral tests. Body weight, glucose, and insulin resistance were monitored. We also measured inflammatory cytokines (interleukin (IL)- 6, IL-1ß, and tumor-necrosis-factor (TNF)-α), an anti-inflammatory cytokine (IL-10), and brain-derived-neurotrophic-factor (BDNF), and glutamate levels in the hippocampus or prefrontal cortex of mice. The findings showed that diabetes increased body weight, glucose, and insulin resistance, impaired working, spatial and recognition memory, increased levels of IL-6, IL-1ß, TNF-α, and glutamate levels, and decreased BDNF in the hippocampus of diabetic mice. While higher physical activity was associated with reduced body weight, glucose, and insulin resistance, attenuated memory impairment, IL-6, IL-1ß, TNF-α, and glutamate, and increased BDNF levels in the hippocampus and prefrontal cortex of diabetic mice. This study shows that swimming training can normalize body weight and glucose-insulin axis and reduce inflammation and glutamate in the hippocampus and enhance the neurotrophic system in both the hippocampus and prefrontal cortex of diabetic mice. This study also suggests that higher physical activity through swimming training can improve cognitive impairment in a mouse model of type 2 diabetes.

Diazepam and exercise training combination synergistically reduces lipopolysaccharide-induced anxiety-like behavior and oxidative stress in the prefrontal cortex of mice.

Anxiety-related disorders are among the most important risks for global health, especially in recent years due to the COVID-19 pandemic. Benzodiazepines like diazepam are generally used to treat anxiety disorders, but the overall outcome is not always satisfactory. This is why psychiatrists encourage patients with anxiety to change their lifestyle habits to decrease the risk of anxiety recurrence. However, the effect of diazepam and exercise in combination is unknown. This study aimed to investigate the effect of diazepam alone or in combination with swimming exercise on lipopolysaccharide (LPS)-induced anxiety-like behavior and oxidative stress in the hippocampus and prefrontal cortex of mice. Mice were exposed to diazepam and swimming exercise alone or in combination with each other and then received LPS. We assessed anxiety-like behavior using open field and light-dark box and measured oxidative markers including glutathione (GSH), malondialdehyde (MDA), and glutathione disulfide (GSSG) in the hippocampus and prefrontal cortex. The findings showed that LPS increased anxiety-related symptoms and oxidative stress by decreasing GSH and increasing MDA and GSSG levels in the prefrontal cortex but not in the hippocampus. Although diazepam alone did not reduce anxiety-like behavior and oxidative stress, it in combination with exercise significantly decreased anxiety-like behavior and oxidative stress in the prefrontal cortex of LPS-treated mice. This drug and exercise combination also displayed a more effective effect in comparison with exercise alone. Overall, this study suggests that diazepam in combination with swimming exercise has higher efficacy on anxiety-like behavior and oxidative stress than when they are used alone.

The role of the oxytocinergic system in the antidepressant-like effect of swimming training in male mice.

Increasing evidence shows that higher physical activity such as running and swimming exercises is associated with decreased depression-related symptoms. However, underlying mechanisms are not fully understood. This study aimed to investigate whether oxytocinergic system can mediate the antidepressant effect of swimming exercises in mice. First, male NMRI mice were subjected to swimming training for eight weeks, then animals intraperitoneally received oxytocin antagonist (L-368899) 1 h before behavioral tests. We assessed anhedonia and social behavior and behavioral despair using the sucrose preference test, social interaction test, and tail suspension test. Oxytocin levels in the brain and serum were also measured. The results showed that swimming training decreased anhedonia and behavioral despair, whereas it increased social behavior and oxytocin levels in male mice. On the other hand, a subthreshold dose of oxytocin antagonist treatment in exercised mice prevented the antidepressant effect of swimming exercise via increased anhedonia and behavioral despair and decreased social behavior compared to the swimming training group. However, the blockade of oxytocin receptors did not affect oxytocin levels in exercised mice. Overall, these findings suggest that oxytocinergic system can play a role in mediating the antidepressant-like effect of swimming training in mice.

Effect of resistance training with and without vitamin D calcium chitosan nanoparticle supplements on apoptosis markers in ovariectomized rats: An experimental study.

Background: Hormone therapy is one of the most effective treatments for menopausal disorders, but it may increase the risk of breast cancer, coronary heart disease, and pulmonary embolism. Objective: The present study investigated the effect of resistance training with and without vitamin D calcium(Ca + + ) chitosan nanoparticles on apoptosis markers in ovariectomized rats. Materials and Methods: 42 female Wistar rats were divided into 7 groups (n = 6/each). One group was assigned as the healthy controls to show the induction of menopause. The other 6 groups comprised ovariectomized (OVX) animals including: 1) vitamin D + calcium + chitosan + resistance training, 2) saline + estrogen + resistance training, 3) saline + resistance training, 4) vitamin D + calcium + chitosan, 5) saline + estrogen, and 6) OVX + control. 48 hr after the last intervention, the hippocampus tissue was extracted to measure the BCL-2-associated X (BAX), B-cell lymphoma 2 (BCL-2), and caspase-3 gene expression as well as the percentage of dead cells. Results: OVX rats demonstrated increased BAX gene expression, ratio of BAX gene expression to BCL-2, caspase-3 gene expression, and percentage of dead cells of hippocampal tissue, but decreased BCL-2 gene expression. Resistance training and vitamin D Ca + + chitosan nanoparticle supplements seemed to reverse these changes. Conclusion: The combination of resistance training and vitamin D Ca + + chitosan nanoparticle supplements may be considered a non-pharmacological treatment for OVX-induced apoptosis.

The effects of aerobic exercise training with octopamine supplementation on cardiomyocyte apoptosis induced by deep-frying oil: The role of caspase and procaspase 3.

BACKGROUND AND AIM: Clinicians who understand how the body responds to exercise, how aerobic training enhances cardiovascular fitness and the benefits and essentials of prescribing aerobic exercise can effectively encourage patients to be active. Deep-frying is a standard cooking method accompanied by the production of carcinogenesis substances such as acrolein. Acrolein is a toxic byproduct of lipid peroxidation involved in the development of pulmonary, cardiac, and neurodegenerative diseases. This study aimed to explore the effect of aerobic exercise (E.X.E.), and octopamine (OCT) on caspase three expression levels in the heart tissue of rats were fed deep-frying oil (D.F.O.). METHODS: 30 male Wistar rats were divided into 5 groups (n = 6 in each) including (1) control (CO), (2) deep-frying oil (DFO), (3) deep-frying oil + exercise (DFO + EXE), (4) deep-frying oil + octopamine (DFO + OCT), and (5) deep-frying oil + exercise + octopamine (DFO + EXE + OCT). The apoptotic effects of D.F.O. in heart tissue were examined by TUNEL assay. Masson's trichrome stain was used to study cardiomyocytic fibers. Moreover, caspase three gene expression in all groups was evaluated using quantitative real-time PCR and the Western blot method. RESULTS: Data showed a significant increase in apoptotic cells in the D.F.O. group (P < 0.05). In Masson's Trichrome stain analysis, more cardiomyocytic fibers degradation and lymphocytic aggregation cells in the DFO + EXE + OCT group significantly improve this degradation. Also, the expression level of caspase 3 was significantly decreased in the DFO + EXE + OCT group (P < 0.05). CONCLUSION: According to the result of the current study, it can be assumed that D.F.O. can lead to programmed cell death via the activation of caspases in heart tissue. However, it seems that aerobic exercise with octopamine supplementation improves heart tissue function by inhibiting the expression of caspase 3 and pro-caspase 3, leading to a significantly decreased apoptosis in cardiomyocytes of DFO-treated models.

Effects of resistance training, palm pollen grain extracts, and testosterone injection on luteinizing hormone receptors, claudin-1, cingulin, and zonula occludens in the prostate tissues of adult male rats.

The present study aimed to investigate the effects of resistance training, Phoenix dactylifera extract, and testosterone enanthate injection on luteinizing hormone receptor, claudin-1, cingulin, and zonula occludens in the prostate tissues of adult rats. 30 male rats were divided into six groups: (1) control, (2) resistance training, (3) Phoenix dactylifera extract, (4) testosterone enanthate, (5) resistance training+Phoenix dactylifera extract, and (6) resistance training + testosterone enanthate. After completing the treatments and resistance training, all rats were sacrificed via anaesthesia. The results showed that resistance training, Phoenix dactylifera, and testosterone enanthate significantly increased the luteinizing hormone receptor, claudin-1, cingulin, and zonula occludens gene expression levels in the prostate. The resistance training treatment, along with Phoenix dactylifera + testosterone enanthate, exerted synergic effects on the prostate luteinizing hormone receptor levels and claudin-1 gene expression. In conclusion, Phoenix dactylifera, as a natural compound with fewer side effects than testosterone injection, can be used to enhance athletic performance. Besides, considering the potential benefits of Phoenix dactylifera, it can be considered in the treatment of testosterone deficiency; however, further research is needed.

The effect of 4-Week rehabilitation by aerobic exercise on hippocampus BDNF and TGF-ß1 gene expressions inAß 1-42-induced rat model of Alzheimer's disease.

Alzheimer's disease (AD) is a type of brain dysfunction featuring a gradual loss in memory. This study aimed to determine the effect of 4 weeks of aerobic rehabilitation exercise (RhExe) on the genes expression of BDNF and TGF-ß1 in the hippocampus tissue of rats with the AD induced by injection of amyloid-beta (Aß1-42). Twenty-one male Wistar rats were randomly divided into 3 groups: Aß injection (n = 7), Aß + exercise (n = 7) and control (n = 7). AD was induced by a single dose of Aß injection into the hippocampus of rats. Three days after surgery, the Aß + exercise group experienced four weeks of the RhExe (5 days/week). Forty-eight hours after the last training session, the animals underwent the Morris water maze test. The animals were sacrificed 24 h after the test, and hippocampal tissue was split. The mRNA expression of BDNF, TGF-ß1, and TGF-ß1 II receptors was measured. The TGF-ß1 and TGF-ß1 II receptor genes expression of Aß + exercise group were significantly higher than the Aß injection group (P ≤ 0.001). BDNF gene expression in the hippocampus of the Aß + exercise group was significantly higher than the Aß injection group (P ≤ 0.001). Spatial memory was significantly higher in the Aß + exercise group than in the Aß injection group (p ≤ 0.01). It seems that aerobic exercise can counteract the harmful effects of Aß through the BDNF and TGF-ß1molecular signaling pathways.

Swimming exercise decreases depression-like behaviour and inflammatory cytokines in a mouse model of type 2 diabetes.

NEW FINDINGS: What is the central question of this study? Can swimming exercise decrease depression-like behaviour and inflammation in type 2 diabetic mice? What is the main finding and its importance? Swimming exercise decreased depression-like behaviour by reducing inflammation in type 2 diabetic mice. Swimming exercise might be useful for the treatment of depression-related disorders in patients with type 2 diabetes. ABSTRACT: Clinical and experimental studies have shown that type 2 diabetes is associated with depression-related disorders. Inflammation has been identified as a common mechanism in both type 2 diabetes and depression. Several studies have suggested that swimming exercise might be able to reduce depression-related symptoms. The present study aimed to explore whether swimming exercise can decrease depression-like behaviour in type 2 diabetic mice. To induce type 2 diabetes, male C57BL6 mice were treated with a high-fat diet and streptozocin. Type 2 diabetic animals were subjected to swimming exercise for 4 weeks. Then, depression-like behaviours were evaluated by sucrose preference, novelty-suppressed feeding, social interaction and tail suspension tests. We also measured levels of glucose, insulin and pro-inflammatory cytokines such as interleukin-1ß and tumour necrosis factor-α in the serum of animals. The results indicated that type 2 diabetes significantly increased anhedonia- and depression-like behaviours in mice. We also found significant increases in glucose, insulin and inflammatory cytokines in diabetic mice. Moreover, swimming exercise reduced anhedonia- and depression-like behaviour in type 2 diabetic mice. Swimming exercise also decreased glucose and inflammatory cytokines in the serum of mice with type 2 diabetes. Collectively, this study demonstrates that swimming exercise decreased depression-like behaviour by reducing inflammation in type 2 diabetic mice. Further clinical studies are needed to validate these findings in patients with type 2 diabetes.

Swimming exercise attenuates anxiety-like behavior by reducing brain oxidative stress in type 2 diabetic mice.

Anxiety-related behaviors are among the most prevalent psychiatric disorders in patients with type 2 diabetes (T2D). The protective effect of exercise on neuropsychiatric disorders has been documented. However, there are no studies that examined whether swimming exercise can decrease anxiety-like symptoms in type 2 diabetes. We investigated the effects of swimming exercise on body weight, anxiety-like behavior, glucose and insulin levels, and brain oxidative stress in male C57BL/6 mice. T2D-induced mice were subjected to swimming exercise, then anxiety-like behaviors were measured by the open field, light-dark box, and elevated plus-maze tests. Glucose and insulin levels were measure in serum, and antioxidant/oxidative markers including glutathione (GSH), malondialdehyde (MDA), and glutathione disulfide (GSSG) were measured in the brain. Our findings showed that T2D increased body weight, anxiety-like symptoms, glucose and insulin resistance, and oxidative stress by increasing MDA and GSSG levels in the brain of mice. Interestingly, swimming exercise reversed these parameters in diabetic mice. Our findings clearly indicate that there is a protective impact of swimming exercise on anxiety-like behavior by reducing insulin resistance and brain oxidative stress in mice with type 2 diabetes. Further studies are needed to validate these findings in humans.

Exercise and fluoxetine treatment during adolescence protect against early life stress-induced behavioral abnormalities in adult rats.

Depression is a psychiatric disorder with several comorbidities that has a complicated pathophysiology. Multiple mechanisms such as abnormal hypothalamic-pituitary adrenal (HPA) axis activity, neurotransmission (namely serotonin), and immune-inflammatory responses are involved in the pathophysiology of disease. In this study, we hypothesized that applying exercise (running wheel (RW) and treadmill (TM)) or fluoxetine (FLX) during adolescence could protect adult rats against the negative impact of early-life stress. To do this, we applied maternal separation stress (MS) to neonatal rats from postnatal day (PND) 2 to 14 and at PND 28, rats were divided into 8 experimental groups and were subjected to TM or RW or FLX treatment. After four weeks of physical activity or FLX treatment, at PND 64, behaviors were assessed by applying forced swimming test, sucrose preference test, open-field test, and elevated plus maze test. Serum cortiscosterone (CORT) levels and expression of genes associated with inflammatory factors (Il1ß, Hmgb1, and Il6) and serotonergic systems (5-ht2c and 5-ht3a) were studies in the hippocampus (HIPP) and prefrontal cortex (PFC). Our results revealed that RW and FLX treatment during adolescence are capable of attenuating MS-induced depressive- and anxiety-like disorders in adult male rats. These effects were accompanied by the normalization of both serum CORT and the expression of genes in the HIPP and PFC. TM exercise in adolescence showed anxiolytic effects but failed to produce antidepressant-like effects. Results of this study suggest that voluntary physical activity during adolescence can reduce the negative effects of early-life stress through different mechanisms.

The effect of regular resistance exercise, vitamin D, and calcium supplements on the gastrocnemius muscle in rats in the post-menopausal period: An experimental study.

BACKGROUND: Menopause is the natural termination of menstruation which affects the quality and important aspects of women's life. OBJECTIVE: To evaluate the effect of regular resistance training (Ex) with vitamin D (Vit. D) and calcium (Ca) supplements in the postmenopausal period on muscle tissue in rats. MATERIALS AND METHODS: In this experimental study, 72 female Wistar rats (8-10-wk old) were randomly divided into control, placebo, Vit. D, Ca, Ex, Ca + Vit. D, Ex + Ca, Ex + Vit. D, and Ex + Ca + Vit. D groups. Control and placebo groups were fed with a standard diet and sesame oil, respectively. Two month after the ovariectomy, Ex, Ca (35 mg/kg), and Vit. D (10000 IU) were administred in all groups except the control. The number of muscle and inflammatory cells, fiber diameter, endomysium thickness, and degenerative collagen fiber area were assessed through hematoxylin-eosin staining. RESULTS: Muscle cell number was increased in the Ex + Vit. D + Ca, Vit. D + Ex, and Vit. D groups compared to the control group; also, inflammatory cell number showed significant increase in the Ex + Vit. D + Ca (12 ± 5.46), Vit. D + Ex (14 ± 3.25), Ex (13 ± 4.08), Vit. D (11 ± 3.26), Ca + Vit. D (10 ± 1.01), and Ca + Ex (9 ± 2.87) groups. Muscle fiber diameter in the Ex + Vit. D + Ca and Vit. D + Ex groups was higher than the other groups. Endomysium thickness was significantly decreased in the Ex + Vit. D + Ca and Vit. D + Ex groups compared to the control and placebo groups (p < 0.001). Degenerative collagen fiber area showed a significant increase in the Ex + Vit. D + Ca and Vit. D + Ex groups (p ≤ 0.001) comparison with the control group. CONCLUSION: Regular resistance exercise, Vit. D, and Ca supplements can improve muscle morphological features in the postmenopausal period.

Effect of regular resistance exercise, vitamin D, and calcium supplements on the bone mineral content and density in postmenopausal model of rats: An experimental study.

BACKGROUND: Postmenopausal osteoporosis progressively occurs due to alteration in the estrogen level during the menopause period, and subsequently elevates the risk of fractures. OBJECTIVE: To evaluate the effect of regular resistance exercise, vitamin D, and calcium supplements on bone mineral content and density, postmenopausal rats used. MATERIALS AND METHODS: In this experimental study, 72 female Sprague-Dawley rats (8-10 wk: 250 ± 15 gr) were ovariectomized and randomly divided into nine groups (n = 8/each): control, placebo, exercise (EX), exercise with vitamin D supplement (EX + D), exercise with calcium (EX + Ca), exercise with calcium and vitamin D (EX + Ca + D), vitamin D administration (D), calcium administration (Ca), and calcium and vitamin D (Ca + D) groups. Finally, the tail, hip, and lumbar bone mineral content, bone mineral density, bone thickness, and bone cells were evaluated in each group. RESULTS: The tail, hip, and lumbar bone mineral density was increased significantly in the EX + Vit D group compared to the control group (p = 0.004, p = 0.007, p = 0.003, respectively). However, there were no significant changes in the bone mineral content of the hips and lumbar among the groups. Besides, bone thickness in the Ex + Vit D group was more than the other groups (p = 0.02). The number of osteoclast cells were decreased in the Ca + Vit D, Ex + Ca, Ex + Vit D, and Ex + Vit D + Ca groups compared to the control group. Osteocyte numbers were increased only in the Ex + Vit D group. CONCLUSION: Resistance exercise in combination with vitamin D and calcium have a positive effect on the bone mineral density and bone mineral content and might be able to prevent or delay the osteoporosis among elderly women. However, additional researches are needed to assess the molecular pathways of this process.

Long-term exercise from adolescence to adulthood reduces anxiety- and depression-like behaviors following maternal immune activation in offspring.

Maternal immune activation is an environmental risk factor for the development of neuropsychiatric disorders such as anxiety and depression later in life. There is an urgent need to develop therapeutic strategies for treating or preventing psychiatric disorders with developmental origins. There is important information that physical exercise is a therapeutic strategy for treating anxiety and depression-related disorders. This study set out to determine the long-term effects of exercise on anxiety and depression-like behaviors following maternal immune activation in adult offspring. Pregnant mice were treated with lipopolysaccharides (LPS) or vehicle. Then offspring were subjected to a combination of different exercise protocols including voluntary running wheel, swimming, and treadmill exercises from adolescence to adulthood. Anxiety and depression-related symptoms in adult offspring were evaluated using open field, elevated plus maze, sucrose preference test, and forced swim test. The hypothalamic-pituitary-adrenal (HPA) axis reactivity was assessed by measuring corticosterone in serum. We also measured oxytocin, malondialdehyde, tumor necrosis factor (TNF)-α, interleukin (IL)-1ß, IL-6, and IL-10 in the brain of adult offspring. Our findings indicated that long-term exercise significantly decreased anxiety- and depression-like behaviors in offspring prenatally exposed to maternal immune activation. The exercise also decreased corticosterone levels in the serum, and increased oxytocin and IL-10 levels in the brain of these offspring; whereas no significant alterations in TNF-α, IL-1ß, IL-6 were found. Taken together, this study suggests that exercise might be a therapeutic strategy for the treatment of anxiety and depression-related behaviors following maternal immune activation in offspring.

The Therapeutic Effect of Exercise on Anxiety and Bowel Oxidative Stress in the Maternal Separation Animal Model.

INTRODUCTION: According to evidence, Early-Life Stress (ELS), mood disorders, and medical comorbidities, i.e. Irritable Bowel Syndrome (IBS), are correlated; however, the direct contribution of ELS to IBS manifestations is less understood. The current study aimed at evaluating the effect of voluntary exercise on the mitochondrial dysfunction of the bowel fibroblasts, following the confirmation of anxiety behavior. METHODS: In this study, Postnatal Day (PND) rats underwent Maternal Separation (MS), as a valid animal model of the brain-gut axis dysfunction, in the days 2-14; three hours daily. On day 21, the study animals were divided into 4 groups, as follows: control, Running Wheel (RW) exercise, MS, and MS+RW groups. The study groups were housed in separate cages (4 rats per cage) until the onset of intervention. On day 60, the elevated plusmaze was used to assess anxiety-like behaviors; the level of oxidative stress biomarkers, i.e. Reactive Oxygen Species (ROS), Glutathione (GSH), as well as Adenosine Triphosphate (ATP) was measured to determine the gut mitochondrial function. RESULTS: Findings revealed that ELS affected the gut energy metabolism in the studied rats; the negative effects of MS on anxiety and the gut mitochondrial dysfunction decreased via RW exercise during adolescence. CONCLUSION: Overall, anxiety behaviors and ROS production, leading to increased GSH and ATP levels, improved after RW exercise; this significantly impacts the function of colon secretory mitochondria. According to the positive effects of RW exercise on mitochondrial dysfunction in an ELS animal model, a potential relationship was found between the brain and gut in the study rats.

Synergic effects of exercise training and octopamine on peroxisome proliferator-activated receptor-gamma coactivator -1a and uncoupling protein 1 mRNA in heart tissue of rat treated with deep frying oil.

Octopamine (OCT) have an adverse effect on heart function. One of the positive effects of exercise training is improving cardiac function and cardiomyocytes signaling, which along with herbal supplements can have better effects on the heart tissue. Therefore, the aim of this study was to evaluate the effects of exercise training and OCT on changes of PGC1α and UCP1 expression in heart tissue of rat treated with deep frying oil (DFO). In this study, 45 male wistar rats were divided into 5 groups (n = 9 in each): I) control (Co), II) DFO, III) DFO + exercise, IV) DFO + OCT, and V) DFO + OCT + exercise. The quantification of apoptotic effects of DFO in heart tissue was assessed by TUNEL assay. Masson's trichrome stain applied to study cardiomyocytic fibers. Moreover, PGC1α and UCP1 genes and proteins expression in all groups were investigated using quantitative real-time PCR and immunohistochemical method. A significant increase in apoptotic cells was observed in the DFO-treated group (p < 0.05). In Masson's Trichrome stain study, more cardiomyocytic fibers were observed and some lymphocytic cells were present in some fibers. Also, the expression of PGC1α and UCP1 was significantly increase in DFO + exercise group, DFO + OCT group, and DFO + OCT + exercise group compare to DFO group (p < 0.05). Based on these findings, exercise and octopamine can be considered as factors affecting the expression of PGC1α genes and UCP1 as well as drug poisoning.

The effect of curcumin and exercise rehabilitation on liver paraoxonase-1 and NF-kß gene expression in the rat induced by forced drinking of ethanol.

AIM OF THE STUDY: Binge ethanol drinking causes liver damage and decreased paraoxonase-1 (PON-1) gene expression. On the other hand, regular physical activity and curcumin consumption as non-invasive interventions can have liver protective effects through enhancing antioxidant defense, and improving PON-1 and NF-kß (nuclear factor kappa B) gene expression. The aim of this study was to investigate the interactive effect of exercise rehabilitation and curcumin consumption on hepatocyte damage as well as NF-kß and PON-1 gene expression in rats. MATERIAL AND METHODS: Fifty-six male Wistar rats were randomly selected and equally divided into seven groups: dextrose-control (Dext-Con), ethanol-control (Eth-Con), ethanol-saline (Eth-sal), ethanol-DMSO (Eth-DMSO), ethanol-curcumin (Eth-Cur), ethanol-swimming training (Eth-SWT) and ethanol-SWT + curcumin (Eth-SWT + Cur). After four days of the binge drinking protocol followed by six days of quitting, the interventions of SWT and curcumin (50 mg/kg) were employed for 14 days. Afterwards, the rats' liver tissues were collected and sent to the laboratory for biochemical assays. RESULTS: The interaction of SWT and curcumin caused an increase in PON-1 gene expression (p = 0.02). In addition, curcumin consumption (p = 0.003) and its interaction with SWT (p = 0.004) resulted in a reduction in NF-kß gene expression. Also, liver tissue damage was observed in the Eth-Con group compared to other groups. CONCLUSIONS: The combination of curcumin and SWT may be used to reduce the side effects of binge ethanol drinking and improve recovery in the quitting period.

The combination of swimming and curcumin consumption may improve spatial memory recovery after binge ethanol drinking.

Helping the return of people with social disorders, including ethanol consumption, are important research topics in the field of biological sciences, and there are many uncertainties about the efficacy of drug interventions and exercise training. The aim of this study was to investigate the effects short-term combination of curcumin and swimming on the improvement of spatial memory. Male Wistar rats (200-250 g) were randomly assigned into ethanol or dextrose groups. After 4 days of gavage, and withdrawn of consumption, they were affected by swimming intervention or curcumin supplementation within 2 weeks. Spatial memory was assessed in Morris Water Maze (MWM) apparatus by a single training session of eight trials. Furthermore, levels of BDNF were measured in hippocampal tissue by doing real time PCR. The results showed that binge ethanol drinking had no significant effect on the traveled distance [F(1,14) = 0.024; P > .05] and escape latency [F(1,14) = 0.648; P > .05] of reaching the platform. In the probe test, both the percentage of swimming time [t(14) = -4.621; P < .001] and distance [t(14) = -4.989; P < .001] in the target quadrant was significantly lower in the ethanol group than the dextrose group. On the other hand in reviewing the effect of curcumin and swimming exercise on learning and spatial memory, The percentage of swimming time was significantly higher in the swim+curcumin [P < .01], training [P < .05] and curcumin [P < .05] subgroups then the control subgroup. The percentage of distance traveled in the swim+curcumin subgroup [P < .001] and curcumin subgroup [P < .05] was significantly higher than the control subgroup. In addition, in the group of binge ethanol drinking, the percentage of swimming time and distance traveled in the target quadrant in the swim+curcumin subgroup was significantly higher than the control subgroup [P < .001]. There was a positive correlation between BDNF gene expression and the percentage of swimming time [P < .01] and the distance traveled in the target quadrant [P < .001] was observed. In conclusion, Binge ethanol drinking causes spatial memory deficiency by reduction of BDNF, and the combination of curcumin and swimming training improves impaired spatial memory after binge ethanol drinking.

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.