Protective effect of alpha-lipoic acid, aerobic or resistance exercise from colitis in second hand smoke exposed young rats.

The role of second hand smoke (SHS) exposure on ulcerative colitis is not known. Our aim was to examine the effects of α-lipoic acid (ALA), chronic aerobic (AE) or resistance exercise (RE) on SHS exposed rats with colitis. Sprague-Dawley male rats (150-200 g, n=54) were selected for colitis induction. Among the colitis groups, one group was exposed to SHS (6 d/wk, 4 cigarettes/d) and the other was not. The SHS group was divided into subgroups as follows: sedentary; AE (swimming; 3 d/wk); and RE (climbing with weight; 3 d/wk). After 5 weeks, colitis was induced by intrarectal acetic acid. All groups had subgroups that were given subcutaneously ALA (50 mg/kg per day) or vehicle for 3 days. Following decapitation, colon tissues were sampled to examine malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity, luminol and lucigenin chemiluminenscence, macroscopic scoring and histologic examination. ANOVA and Student's t-test were used for statistical analysis. The increased macroscopic and microscopic scores, MPO, MDA, luminol and lucigenin measurements in colitis and SHS-colitis groups were decreased via ALA (P<.05-.001). AE declined macroscopic and microscopic scores, MDA, lucigenin compared to colitis and SHS-colitis groups (P<.01-.001). RE reduced microscopic score, MPO, MDA, luminol, lucigenin (P<.05-.001) that were increased with colitis. Decreased GSH levels (P<.01) in the SHS-colitis group approached to control levels when given ALA. According to our results SHS and colitis induction increased inflammatory damage. SHS did not worsen it more than colitis. Our results suggest that ALA, AE or RE might be protective for SHS exposed ulcerative colitis conditions.

Effects of MC4R, FTO, and NMB gene variants to obesity, physical activity, and eating behavior phenotypes.

Obesity is a major contributory factor of morbidity and mortality. It has been suggested that biological systems may be involved in the tendency to be and to remain physically inactive also behaviors such as food and beverage preferences and nutrient intake may at least partially genetically determined. Consequently, besides environment, genetic factors may also contribute to the level of physical activity and eating behaviors thus effect obesity. Therefore the aim of this study is to investigate the effect of various gene mutations on obesity, physical activity levels and eating behavior phenotypes. One hundred patients and 100 controls were enrolled to the study. Physical activity levels were measured with an actical acceloremeter device. Eating behaviors were evaluated using Three-Factor Eating questionnaire (TFEQ). Associations between eating behavior scores and physical characteristics were also evaluated. The information about other obesity risk factors were also collected. Mutations were investigated with PCR, direct sequencing and Real-Time PCR. rs1051168, rs8050146 -2778C > T mutations were found statistically significant in patients, rs1121980 was found statistically significant in controls. 21 mutations were found in MC4R and near MC4R of which 18 of them are novel and 8 of them cause amino acid change. In addition, it was found that, some obesity related factors and questions of TFEQ are associated with various investigated gene mutations. Any relation between gene mutations and physical activity levels were not detected. It is thought that, due to the genotype data and eating behaviors, it may be possible to recommend patients for proper eating patterns to prevent obesity. © 2016 IUBMB Life, 68(10):806-816, 2016.

Estrogen receptor agonists alleviate cardiac and renal oxidative injury in rats with renovascular hypertension.

Although endogenous estrogen is known to offer cardiac and vascular protection, the involvement of estrogen receptors in mediating the protective effect of estrogen on hypertension-induced cardiovascular and renal injury is not fully explained. We aimed to investigate the effects of estrogen receptor (ER) agonists on oxidative injury, cardiovascular and renal functions of rats with renovascular hypertension (RVH). Female Sprague-Dawley rats were randomly divided as control and RVH groups, and RVH groups had either ovariectomy (OVX) or sham-OVX. Sham-OVX-RVH and OVX-RVH groups received either ERß agonist diarylpropiolnitrile (1 mg/kg/day) or ERα agonist propyl pyrazole triol (1 mg/kg/day) for 6 weeks starting at the third week following the surgery. At the end of the 9(th) week, systolic blood pressures were recorded, cardiac functions were determined, and the contraction/relaxation responses of aortic rings were obtained. Serum creatinine levels, tissue malondialdehyde, glutathione, superoxide dismutase, catalase levels, and myeloperoxidase activity in heart and kidney samples were analyzed, and Na(+), K(+)-ATPase activity was measured in kidney samples. In both sham-OVX and OVX rats, both agonists reduced blood pressure and reversed the impaired contractile performance of the heart, while ERß agonist improved renal functions in both the OVX and non-OVX rats. Both agonists reduced neutrophil infiltration, lipid peroxidation, and elevated antioxidant levels in the heart, but a more ERß-mediated protective effect was observed in the kidney. Our data suggest that activation of ERß might play a role in preserving the function of the stenotic kidney and delaying the progression of renal injury, while both receptors mediate similar cardioprotective effects.

High intensity interval training protects from Post Traumatic Stress Disorder induced cognitive impairment.

This study aimed to show the possible protective effects of high intensity interval training (HIIT) in PTSD-induced rats and probable underlying mechanisms. Female rats (n = 44) were separated as; Sedentary (SED), moderate intensity continuous training (MICT), HIIT groups. Then the groups were divided into subgroups according to PTSD induction (n = 6-8/group). Exercise groups performed HIIT or MICT for 6 weeks. On the fifth week, PTSD was induced by single prolonged stress protocol. Cognitive functions were evaluated by object recognition, anxiety levels by hole-board and elevated plus maze, and fear conditioning by passive avoidance tests. Following decapitation, malondialdehyde (MDA), glutathione (GSH), luminol and lucigenin chemiluminescence levels, and myeloperoxidase (MPO), superoxide dismutase (SOD) and catalase (CAT) activities were measured, and histopathological damage was evaluated. The data was analyzed by one-way ANOVA. Cognitive decline and aggravated anxiety levels in SED + PTSD group were improved in both PTSD-induced exercise groups (p < 0.05-0.001). The increased chemiluminescence levels, MPO activity and histological damage were depressed in both PTSD-induced exercise groups (p < 0.05-0.001). The risen MDA levels in SED + PTSD group were suppressed only in HIIT + PTSD group (p < 0.01-0.001). The decreased GSH levels were increased by MICT (p < 0.05-0.001), and CAT and SOD activities were improved via HIIT (p < 0.05). Compared to SED group, latency was decreased in SED + PTSD (p < 0.05-0.01) group. Neuronal damage scores were alleviated in both PTSD-induced exercise groups (p < 0.001). PTSD-induced memory decline was protected by both of the exercise models however more effectively by HIIT via decreasing oxidative stress, anxiety levels and by improving antioxidant capacity as a protective system for neuronal damage.

Protective effects of different exercise modalities in an Alzheimer's disease-like model.

Our aim was to investigate the probable protective effects of aerobic, resistance and combined exercise methods on ovariectomy and d-galactose induced Alzheimer's Disease (AD)-like model. d-galactose (100mg/kg) or saline were administered intraperitoneally for 6 weeks to ovariectomized or sham-operated rats (n=8/group). Aerobic (AE), resistance (RE) and combined exercises (CE) (aerobic+resistance) were performed for 3 times a week for 6 weeks. Anxiety level and cognitive functions were evaluated via hole-board and object recognition tests. Brain myeloperoxidase, malondialdehyde, nitric oxide activity, lucigenin-enhanced chemiluminescence, glutathione and serum insulin like growth factor-I (IGF-I) assays were done. Hippocampal mRNA levels of nerve growth factor (NGF), brain derived neurotrophic factor (BDNF), and amyloid precursor protein 695 (APP695) were measured. Amyloid Beta (Aß), NGF, BDNF, IGF-I immunoreactive neurons were evaluated. Freezing time were increased in AD-like model and decreased back with AE (p<0.05). Deteriorated working memory in AD-like model was improved with all exercise types (p<0.05-0.001). Reduced glutathione levels in AD-like model were increased and increased malondialdehyde levels were reduced and serum IGF-I levels were increased by all exercises (p<0.05-0.001). Increased APP mRNA levels in AD-like model were decreased via CE (p<0.05). Elevated Aß scores in AD-like model were decreased by RE and CE (p<0.01) in hippocampus and by all exercise types in cortex (p<0.05-0.01). Decreased cortical NGF immunocytochemical scores of AD-like model were increased by CE (p<0.05). Different exercise models may have protective effects in development stage of AD via reducing oxidative stress and Aß scores, and by improving antioxidant system and brain plasticity.

Effect of moderate or high intensity exercise on hypothyroid rats exposed to acute stress.

BACKGROUND: There are contradictory results about stress response in hypothyroidism and in exercising with variant intensities. We aimed to investigate the potential anxiolytic and protective effects of different intensities of exercise on acute psychological stress in hypothyroidism. METHODS: Rats (N.=48) were divided as sedentary, moderate intensity (MIE) and high intensity exercise (HIE) groups. Rats were administered intraperitoneally with 6-n-propyl-2-thiouracil (PTU, 10 mg/kg) for 15 days to induce hypothyroidism. Starting by the 3rd week, treadmill exercise was performed moderately (30 min/day) or at high intensity (60 min/day) for 6 weeks, 5 days/week. At the end of the 8th week, exposure to water avoidance stress was used for induction of acute stress. Anxiety-like behavior was determined by holeboard test before and after stress inductions. Serum IL-1ß and IL-6 assays, and myeloperoxidase activity (MPO), malondialdehyde (MDA), and glutathione (GSH) measurements, and histological analysis of heart, liver, stomach and small intestine were made. RESULTS: All groups showed increased anxiety-like behavior following acute stress induction. After acute stress induction, increased MPO and MDA levels in heart and elevated MPO activity in liver were inhibited in PTU-treated HIE group. In MIE rats, increased MPO and declined GSH levels of the gastric tissue and small intestine, and elevated MDA levels of gastric tissue were reversed in PTU-treated MIE group. Major histological changes that occurred by both intensities of exercise under stress condition were improved by PTU. CONCLUSIONS: Our results indicate that hypothyroid state may be protective against stress- and exhaustive exercise-induced oxidative damage.

Protective effect of low dose caffeine on psychological stress and cognitive function.

INTRODUCTION: Caffeine is an adrenergic antagonist that enhances neuronal activity. Psychological stress depresses cognitive function. AIM: To investigate the effects of acute and chronic low dose caffeine on anxiety-like behavior and cognitive functions of acute or chronic psychological stressed rats. MATERIAL-METHOD: Acute or chronic caffeine (3mg/kg) was administered to male Sprague Dawley rats (200-250g, n=42) before acute (cat odor) and chronic variable psychological stress (restraint overcrowding stress, elevated plus maze, cat odor, forced swimming) induction. Anxiety and cognitive functions were evaluated by hole-board and object recognition tests. The brain glutathione and malondialdehyde assays, myeloperoxidase, nitric oxide (NO), superoxide dismutase (SOD), luminol and lucigenin activity and histological examination were done. ANOVA and Student's t-test were used for statistical analysis. RESULTS: The depressed cognitive function with chronic stress exposure and the increased anxiety-like behavior with both stress inductions were improved via both caffeine applications (p<0.05-0.001). Both caffeine pretreatments in chronic stressed rats, and chronic caffeine in acute stressed ones reduced the elevated myeloperoxidase activities (p<0.05-0.01). The increased malondialdehyde, lucigenin and NO levels with acute stress were inhibited with chronic caffeine (p<0.05-0.01), malondialdehyde and NO levels were declined by acute caffeine (p<0.001). Acute caffeine decreased SOD activity (p<0.01) and improved glutathione (p<0.01) and luminol levels (p<0.05). The induced histological damage with both stress exposures was ameliorated with chronic caffeine. CONCLUSION: The increased anxiety-like behavior and depleted cognitive functions under stress conditions were improved with both acute and predominantly chronic caffeine pretreatments by decreasing oxidative damage parameters.