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This study investigated the possible protective and therapeutic effects of Myrtus communis subsp. communis ethanol extract (MC) in aluminum chloride (AlCl3) and D-galactose (D-Gal) induced Alzheimer's disease in rats. MC was orally given to rats as a protective treatment for 90 days and, in other two groups starting from the 60th day MC (100-200 mg/kg) was administered, concomitantly with AlCl3 and D-Gal. Learning and memory functions were evaluated by the behavioral tests. Biological activities of MC treatment were examined in hippocampal tissues by ELISA tests. D-Gal and AlCl3-treated rats showed increased amyloid beta (Aβ) and 8-hydroxy-2-deoxyguanosine (8- OHdG) levels, acetylcholinesterase activity and decreased neprilysin, Na+-K+ATPase and SOD levels in parallel with a decrease in Novel Object Recognition Test, Morris Water Maze and Passive Avoidance Test scores. On the other hand, MC administration reversed the behavioral impairments and improved learning and memory. Moreover, MC treatment decreased Aβ and 8-OHdG levels and acetylcholinesterase activity and increased neprilysin levels, Na+-K+ATPase and SOD levels. Our results suggest that MC has beneficial effects on cognitive and neuronal functions through its anticholinesterase and antioxidant properties. [ABSTRACT FROM AUTHOR]

Alzheimer's disease is a challenging disease for patients due to progressive loss of cognition and behavioral disorders. Disruption of cholinergic transmission and neuroinflammation are the most important mechanisms underlying cognitive damage. Beta vulgaris L. var. cicla (BV) has been reported to have various pharmacological effects associated with its rich antioxidant content. In addition, anticholinesterase and antiinflammatory activities of BV have been demonstrated in vitro. The aim of this study is to elucidate the therapeutic effect of BV against cognitive impairment, reduction in cholinergic transmission and neuroinflammation caused by intracerebroventricular (ICV) administration of streptozotocin (STZ). STZ was administered bilaterally at a dose of 3 mg/kg via ICV to rats, and BV treatment at a dose of 2 g/kg for 21 days was administered orally to STZ-induced animals. After behavioral tests, AChE activity, TNF-α and IL-1β levels were measured in hippocampus and cortex tissues excised from decapitated animals. Novel object recognition and passive avoidance test showed that the treatment of BV reverted the ICV-STZ induced memory dysfunctions in rats. Furthermore, increased AChE levels in the hippocampal and cortical tissues of STZ-induced rats were significantly reduced with 21 days of BV treatment. In conclusion, these results confirm that STZ administration caused cholinergic hypofunction, neuronal inflammation and cognitive dysfunction in rats, and BV therapy significantly inhibited these changes with its potential neuroprotective activity. [ABSTRACT FROM AUTHOR]

Obesity causes cognitive weakening and increases the risk of neurodegenerative diseases. Myrtus communis extract (MC) has anti-inflammatory and antioxidant properties. In this study, it is aimed to investigate the effects of Myrtus communis on oxidative brain damage caused by a high-fat diet (HFD), using behavioral and biochemical parameters. Twenty-four Wistar albino rats (200-250 g) were divided into three groups. The control group (C) received a standard diet, while HFD groups were received HFD for 16 weeks. MC (100 mg/kg, oral) was given to the HFD + MC group for the last 4 weeks. At the end of the study, the novel object recognition test (NORT) was performed and the hippocampus and blood samples were collected. Acetylcholinesterase (AChE) and Na+/K+- ATPase activities, malondialdehyde (MDA), 8-hydroxy-2'-deoxyguanosine (8-OHdG) and reduced glutathione (GSH) levels were measured in the hippocampal samples and cholesterol levels were analyzed in sera. Findings have shown that NORT performance of the HFD group was reduced, while administration of MC prevents this reduction and in parallel, increased AChE and decreased Na+/K+ -ATPase activities were ameliorated by administration of MC. Increased MDA and 8-OHdG levels observed in the HFD group, were decreased in the MC treated HFD group. Our results point out that MC has ameliorative effects on hippocampal oxidative stress and cognitive impairment in high fat nutritioninduced obesity. [ABSTRACT FROM AUTHOR]

Cisplatin is a chemotherapeutic agent that is the first to enter treatment from organic platinum-derived drugs. Nephrotoxicity and cytotoxicity are major factors that limit its use. The aim of the study is to investigate the possible protective effects of quercetin against cisplatin-induced urogenital organ toxicity. In our study, Sprague Dawley four month old male rats were divided into 4 groups; control + saline (SF), control + quercetin (20 mg/kg for 21 days), cisplatin (7 mg/kg as a single dose) + SF and cisplatin + quercetin groups. After decapitation, the kidney, bladder, testis and corpus cavernosum tissue samples were taken to analyze caspase-3, an index of apoptosis, and oxidative stress parameters such as malondialdehyde (MDA), gluta-thione (GSH), and 8-hydroxy-2' -deoxyguanosine (8-OHdG). Furthermore, tissues were also examined histologically. Cisplatin caused significant increases in MDA and 8-OHdG levels, demonstrating increases in lipid peroxidation and oxidative DNA damage, respectively, in all tissues. In parallel with the oxidant stress increase, the endogenous strong antioxidant GSH levels were decreased. Caspase activity and caspase 3 expressions, which we measured as an indicator of apoptosis, increased significantly with cisplatin treatment. On the other hand, treatment with quercetin, a powerful antioxidant flavonoid, reversed these changes. Histological findings also demonstrated well-preserved tissues due to quercetin treatment. In conclusion, our results suggested that quercetin, when given with cisplatin, can be protective against the chemotherapeutic induced toxicity and thus provide therapeutic benefit. [ABSTRACT FROM AUTHOR]

The aim of this study was to investigate the effects of calorie restriction (CR) and swimming exercise (SW) on oxidative injury in kidney and bladder tissues, in rats with metabolic syndrome (MS). 3-months old rats were divided into five; Control, MS, MS+CR, MS+SW, MS+CR+SW. The metabolic syndrome model was created using 10% fructose solution in drinking water for three months. Afterwards, SW and 40% CR were applied for six weeks. Blood glucose measurements were performed at the beginning, the third month and the end of experiment. After decapitation, blood, kidney and bladder samples were collected. Cytokine levels, antioxidant and oxidative stress parameters were examined. There was a remarkable change in blood glucose levels in MS+CR+SW group. Fructose-induced increased TNF-a and decreased ADP levels in plasma were reversed in CR, SW, and CR+SW groups. MDA levels were increased, while SOD and ADP levels were decreased in renal and bladder tissues in MS group. CR and SW significantly reversed all parameters in both tissues. Moreover, caspase activity increased in both tissues in MS group. CR decreased the caspase activity in kidney tissue, and in bladder tissues caspase activity significantly decreased with both CR and SW. Western blot analysis showed an increased caspase-3 protein expression in both tissues which was reversed by CR, SW, and CR+SW. The results of our study showed that MS disrupts the balance of pro/anti-inflammatory cytokines in plasma and causes oxidant damage in urinary tissues. Calorie restriction and exercise are protective against the damage caused by MS. [ABSTRACT FROM AUTHOR]

Nephrolithiasis is common urological problem and stone formation has multiple underlying pathogenetic factors. We investigated the possible preventive and therapeutic effects of Urtica dioica ethanol extract (UD) on ethylene glycol-induced nephrolithiasis model in rats. Sprague-Dawley rats were divided into four groups (n = 10). The control group was given normal drinking water for 8 weeks and was administered vehicle by gastric gavage. Stone formation was induced by adding 0.75% ethylene glycol (EG) to their drinking water. UD (700 mg/kg) was given orally for 8 weeks to the preventive group and for last 4 weeks to the treatment group, respectively. At the end of the experiment, urine, blood samples and kidney tissues were obtained. In 24-hour urine samples, calcium and citrate levels were decreased and oxalate levels were increased in EG group whereas UD treatment groups reversed these parameters back to control levels. In addition, serum levels of creatinine and urea were increased in EG group, while UD significantly reduced these parameters. Malondialdehyde, 8-hydroxydeoxyguanosine and tumor necrosis alpha levels, and caspase- 3 and N-acetyl-β-glucosaminidase activities were elevated in EG group and showed a decrease in UD treated groups. Glutathione level was decreased in EG group, whereas it was increased in UD preventive group. Histological examination showed an improvement in UD treated groups. Our results suggest that UD is effective both in prevention and treatment for kidney stones. The mechanism underlying this effect may be the antioxidant effect of UD and the effect on the concentration of stone-forming components in the urine. [ABSTRACT FROM AUTHOR]

Aging is a progressive and catabolic process by cells of the body are broken down. Study scrutinized the effects of exercise and caloric restriction in cardiovascular hemodynamics and antioxidant system parameters. Rats divided to 5 categories as 1 control group (including 3 months aged animals) and 4 test groups (including 15 months aged animals) named by A-SED (aged-sedentary), A-CR (aged-caloric restricted), A-EX (aged-exercised) and A-CR-EX (aged-(exercised + caloric restricted)) created by adding carbachol (CAR) and phenylephrine (PE) cumulatively and during 6 weeks, 40% caloric restriction and swimming were administered to aged animals. At the beginning and end of study, blood pressure (BP) and ECHO of the animals were measured. After decapitation process, tissue (heart and aorta) samples were collected. In tissue samples, apoptotic and oxidative stress parameters, and in blood samples NO levels were studied. Additionally, tissues were viewed as histologically at light microscopy. GraphPad Prism 5v. program was used for statistics and p<0.05 were considered significantly. Contraction-relaxation responses of aorta improved after CR and EX administrations (p<0.05). In both tissues, oxidative stress parameters (8-OHdG, MDA, SOD, GSH), caspase-3 activity and caspase-3 dansity were recovered meaningfully (p<0.05). Finally, NO levels were significantly recovered with CR and EX administrations in aged animals (p<0.05). To sum up, it is suggested that CR and EX administrations contribute to the recovery of hemodynamic and antioxidant system parameters in aged rats. [ABSTRACT FROM AUTHOR]

In renovascular hypertension (RVH), oxidative stress and inflammation due to high blood pressure and elevated levels of angiotensin 2 are mainly responsible of cerebrovascular complications and impaired cognitive functions. Since the nicorandil has been shown to exert neuroprotective, anti-inflammatory and antioxidant effects, we investigated the effect of nicorandil against vascular dementia and blood brain barrier damage in a rat model of angiotensin-dependent hypertension. Wistar albino rats, were divided as sham-operated control, renovascular hypertension (RVH) and Nicorandil-treated RVH groups. Silver clip was implanted onto the left renal artery. Using the tail-cuff method, blood pressure of rats was measured before the surgery and at the end of the post-surgical 3rd and 12th weeks. Nicorandil (4mg/kg, orally) or vehicle was administered for 9 weeks. Twelve weeks after RVH surgery, a new object recognition test was performed. Following the determination of blood brain barrier integrity, serum samples were taken for the evaluation of proinflammatory cytokines tumor necrosis alpha (TNF-α) and interleukin-1 beta (IL- 1β). Levels of sodium-potassium adenosine triphosphatase (Na+/K+-ATPase), as a marker of endothelial damage, were evaluated in the hippocampal tissues. RVH resulted in significant increases in TNF-α and IL-1β levels and decreases in Na+/K+-ATPase levels, along with impairment in blood brain barrier integrity and memory performance. In the nicorandil treatment group, these indices were reversed back to control levels. The present data demonstrated that nicorandil attenuates RVH-induced memory impairment and blood brain barrier damage in rats with RVH. [ABSTRACT FROM AUTHOR]

Reactive oxygen metabolites play important roles in ischemia/reperfusion (I/R) injury in several organ systems. Riboflavin has been shown to exert antioxidant and/or anti-inflammatory activities in several experimental models. The aim of this study was to investigate the role of riboflavin against I/R injury in the rat kidney. Wistar albino rats 200-300 g weighing were divided into 3 groups. One week after unilateral nephrectomy, the IR procedure was applied to the rats. To induce I/R injury renal pedicle was clamped for 45 minutes and then rats were allowed reperfusion for 6 hours. Riboflavin (25 mg/kg, orally) or vehicle was administered for one week as pretreatment. After decapitation, kidney tissue samples were taken for the evaluation of malondialdehyde (MDA), an end product of lipid peroxidation; glutathione (GSH), a key antioxidant; and 8-hydroxydeoxyguanosine (8-OHdG), a specific marker of oxidative DNA damage. Furthermore, myeloperoxidase (MPO) and caspase-3 activities were also examined together with histological analysis. Ischemia/reperfusion induced significant increases in MDA and 8-OHdG levels and MPO and caspase- 3 activities, and decrese in GSH levels. In the riboflavin treatment these indices were found to be reversed back to control levels. The present data demonstrated that riboflavin, through its antioxidant effect, attenuates I/R induced acute renal injury in rats. [ABSTRACT FROM AUTHOR]