Dilek Özbeyli

Protective effect of exercise and sildenafil on acute stress and cognitive function.

INTRODUCTION There are contradictory results about the effects of exercise and sildenafil on cognitive functions. AIM To investigate the effects of sildenafil pretreatment and chronic exercise on anxiety and cognitive functions. METHOD Wistar rats (n=42) were divided as sedentary and exercise groups. A moderate-intensity swimming exercise was performed for 6 weeks, 5 days/week, 1h/day. Some of the rats were administered orogastrically with sildenafil (25mg/kg/day) either acutely or chronically. Exposure to cat odor was used for induction of stress. The level of anxiety was evaluated by elevated plus maze test, while object recognition test was used to determine cognitive functions. Brain tissues were removed for the measurement of myeloperoxidase (MPO), malondialdehyde (MDA), nitric oxide levels, lucigenin-enhanced chemiluminescence, and for histological analysis. RESULTS Increased MPO and MDA levels in sedentary-stressed rats were decreased with sildenafil applications. Chronic exercise inhibited the increase in MPO levels. Increased nitric oxide and lucigenin chemiluminescence levels in sedentary-stressed rats, were diminished with chronic sildenafil pretreatment. The time spent in the open arms of the plus maze was declined in sedentary-stressed rats, while chronic sildenafil pretreatment increased the time back to that in non-stressed rats. Acute sildenafil application to exercised rats prolonged the time spent in open arms as compared to non-treated exercise group. The time spent with the novel object, which was decreased in sedentary-stressed rats, was increased with sildenafil pretreatment. Our results suggest that sildenafil pretreatment or exercise exerts a protective effect against acute stress and improves cognitive functions by decreasing 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 Students 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.

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

HighlightsAerobic exercise improves anxiety‐like behaviour in an Alzheimer’s disease‐like model.Aerobic, resistance and combined exercises protect from oxidative stress and memory decline.Exercise has neurotrophic effects.Exercise decreases A&bgr; burden in developmental stage of Alzheimer’s disease‐like conditions. ABSTRACT 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 (100 mg/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 (A&bgr;), 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 A&bgr; 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 A&bgr; scores, and by improving antioxidant system and brain plasticity.

Effects of Ovariectomy and Estrogen Replacement Therapy on Laryngeal Tissue A Histopathological Experimental Animal Study

Objective. To determine the histopathological effect of estrogen deficiency and hormone replacement treatment on laryngeal tissue in ovariectomized rats. Study Design. Animal study. Setting. The study was conducted at the animal experiment laboratory of Marmara University School of Medicine, Istanbul, Turkey. Subjects and Methods. Six-month-old female Wistar albino rats were divided into the following 3 groups (n = 8 per group): sham-operated control, ovariectomized, and ovariectomized with estrogen replacement. Rats in the ovariectomized with estrogen replacement group received 17 β-estradiol valerate (200 µg/kg, subcutaneously) once a week. Animals were killed after 8 weeks of intervention. Results. Significant changes were observed in the ovariectomized group when edema in lamina propria, inflammation in squamous, respiratory epithelia and lamina propria, pseudostratification, and cilia loss were assessed. Except cilia loss, there were no significant differences in the assessments between the sham-operated control and ovariectomized with estrogen replacement groups. Conclusions. On the basis of histopathological evaluations, it was shown that estrogen replacement helped to improve laryngeal changes due to experimentally induced menopause.

Treatment with milk thistle extract (Silybum marianum), ursodeoxycholic acid, or their combination attenuates cholestatic liver injury in rats: Role of the hepatic stem cells

BACKGROUND/AIMS Cholestasis, which results in hepatic cell death, fibrosis, cirrhosis, and eventually liver failure, is associated with oxidative stress. The aim of this study was to evaluate the effects of milk thistle (MT, Silybum marianum) and ursodeoxycholic acid (UDCA) or their combination on the activation of hepatic stem cells and on the severity of cholestasis liver injury in rats. MATERIALS AND METHODS Under anesthesia, bile ducts of female Sprague Dawley rats were ligated (BDL) or had sham operation. BDL rats were administered saline, UDCA (15 mg/kg/d), MT (600 mg/kg/d), or UDCA+MT by gavage for 10 days. On the 11th day, rats were sacrificed and blood and liver samples were obtained. Serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), hepatic malondialdehyde (MDA) levels, and myeloperoxidase (MPO) activity were measured. Hepatic injury, a-smooth muscle actin expression, and stem cell markers c-kit, c-Myc, Oct3/4, and SSEA-1 were histologically determined. RESULTS Histological scores, serum ALT, and hepatic MDA levels were higher in BDL group than in the sham rats, while all treatments significantly reduced these levels. The reduction in ALT was significantly greater in UCDA+MT-treated group than in other treatment groups. c-Kit, c-Myc, Oct3/4, and SSEA-1 were increased in saline-treated BDL group with respect to sham-operated control group, and these markers were significantly reduced in all treatment groups. CONCLUSION In addition to a modulatory effect on the stem cell-induced regenerative response of the liver, UDCA, MT, and their combination demonstrated similar anti-inflammatory and antiproliferative effects on cholestasis-induced hepatic injury.

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 Students 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.

Protective Effect of Nicotine on Sepsis-Induced Oxidative Multiorgan Damage: Role of Neutrophils

Introduction Despite its adverse health consequences, tobacco smoking is associated with lower incidence of several neurodegenerative and inflammatory diseases. The present study is aimed to show the effects of nicotine, major tobacco constituent, on five organs targeted by sepsis. Methods Male Wistar albino rats received tap water with (5mg/kg) or without nicotine for 14 days. Under ketamine anesthesia, sepsis (n = 50) was induced by ligation and puncture of the cecum, while sham group (n = 8) had only laparotomy. In other rats, nicotine drink was withdrawn for 5 days before sepsis induction, while in acute nicotine group, rats were injected with nicotine (30mg/kg, i.p.) before sepsis, but had no oral intake. Rats were decapitated 24 hours after surgery to obtain lung, liver, ileum, heart, and kidney tissues to determine malondialdehyde (MDA) and glutathione (GSH) levels and myeloperoxidase (MPO) activities. Data were analyzed by one-way analysis of variance and Tukey multiple comparison tests or Students t test. Results Chronic nicotine administration or its withdrawal reduced lipid peroxidation and MPO activity and prevented GSH depletion with some varying results in different target tissues. Nicotine injection prior to sepsis depressed MPO activity in all tissues and reduced MDA levels except for the lung, while GSH levels were elevated only in the hepatic and ileal tissues. Histologically observed injury was ameliorated by all nicotine treatments at varying degrees. Conclusions The findings of the present study indicate that long-term nicotine administration reduces sepsis-induced oxidative damage in several tissues, which appears to involve inhibition of neutrophil activity in the inflamed tissues. Implications Nicotine administration or its withdrawal reduced lipid peroxidation and neutrophil content and prevented GSH depletion with some varying results in different target tissues. A single injection prior to sepsis induction depressed MPO activity in all the tissues and reduced all tissue MDA levels except for the lung. When nicotine was withdrawn for 5 days, its inhibitory effect on MPO activity was still present in all the tissues except for the liver. Microscopically an improved inflammatory response was observed in all the tissues of rats that have received different nicotine pretreatment regimens.

Evaluation of the Effectiveness of Esterified Hyaluronic Acid Fibers on Bone Regeneration in Rat Calvarial Defects

Hyaluronic acid (HA) constitutes one of the major components of the extracellular matrix domain in almost all mammals. The aim of this study was to evaluate the regenerative capacity of HA matrix in rat calvarial bone defects and compare with those of different combinations of resorbable collagen membrane (M) and bovine-derived xenograft (G). Twenty-four 3-month-old male Sprague-Dawley rats weighing 200-250 g were included. Control group was created by leaving one defect empty from 2 critical size defects with 5 mm diameter formed in the calvarial bones of 8 rats. In the same rats, the other defect was treated with HA matrix alone. One of the 2 defects formed in other 8 rats was treated with HA+G and the other with HA+M. One of the 2 defects formed in the remaining 8 rats was treated with G+M and the other with HA+G+M. The animals were sacrificed at 4 weeks. Histologic, histomorphometric, and immunohistochemical analyses were performed. Both HA matrix alone and its combinations with G and M supported new bone formation (NBF). However, NBF was significantly greater in G+M and HA+G+M groups compared to control and HA alone (P<0.001). Bone morphogenetic protein-2 was expressed with varying degrees in all groups, without any difference among them. Within the limitations of the present study, HA matrix, used alone or in combination with G and M, did not contribute significantly to bone regeneration in rat calvarial bone defects.

The effects of lipoic acid and methylprednisolone on nerve healing in rats with facial paralysis

Abstract Objective: To investigate the effects of lipoic acid and methylprednisolone on nerve healing in rats with traumatic facial paralysis. Materials and methods: The rats were randomly divided into four groups, with six rats in the control group and eight each in the remaining three groups. The buccal branch of the facial nerve in all groups except the control group was traumatized by a vascular clamp for 40 minutes. Group 1 was given lipoic acid (LA), Group 2 was given methylprednisolone (MP), and Group 3 was given lipoic acid and methylprednisolone (LA + MP) for one week. Nerve stimulus thresholds were measured before trauma, after trauma and at the end of the one week treatment period. Results: When the groups were compared with each other, post-treatment threshold levels of LA + MP were significantly lower than LA. Although post-treatment threshold levels of LA and MP were still higher than the control group, there was no significant difference between LA + MP and control values (p > .05). Conclusion: Lipoic acid has a positive effect on nerve healing and can enhance the effect of methylprednisolone treatment. It is a good alternative in cases where methylprednisolone cannot be used.