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WOS: 000404317300028 PubMed: 28576521 Objective: To investigate the effects of caffeic acid phenethyl ester (CAPE) on tympanosclerosis. Materials and methods: Thirty-two male Sprague Dawley rats were separated into 4 groups as CAPE (n = 10), alcohol (n = 10), control (n = 8) and normal (n = 4) groups. All tympanic membranes except normal group were myringotomised and type 3 Streptococcus pneumoniae strains was injected into their middle ears. Myringotomies were repeated for 5 weeks. Intraperitoneal (i.p) CAPE were administrated to the CAPE group at 10 mu mol/kg/day and 10% ethyl alcohol administrated to the alcohol group for 5 weeks. The control group were left untreated. Findings of myringosclerosis were recorded by otomicroscope at sixth week. Then, all rats were sacrificed and tympanic membrane thickness and severity of middle ear mucosal inflammation evaluated histopathalogically. Results: Severity of myringosclerosis was significantly higher in the alcohol and control groups compared to the CAPE group (p < 0.001), but was not significant when alcohol and control groups were compared (p = 0.17). The tympanic membrane thickness measured in the alcohol and control groups were significantly higher compared to the CAPE group (p < 0.001), but was not significant when alcohol and control groups were compared (p = 0.17). The severity of inflammation in the middle ear mucosa was significantly higher in the alcohol and control groups compared to the CAPE group (respectively, p < 0.001, p = 0.03). The severity of inflammation in the middle ear mucosa was not significant between alcohol and control groups (p = 0.30). Conclusion: CAPE has anti-inflammatory and antioxidant effects on the development of MS in myringotomized rats, so reduces the severity of tympanosclerosis. (C) 2017 Elsevier B.V. All rights reserved. Samsun Training and Research Hospital This work was supported by the Samsun Training and Research Hospital.

Ozdemir, Dogukan/0000-0003-2008-163X WOS: 000496853000005 PubMed: 31351349 Objectives: Myringosclerosis commonly occurs as a long-term complication of ventilation during the treatment of otitis media. We aimed to determine the effects of rosmarinic acid as an antioxidant on experimentally induced myringosclerosis. Methods: Twenty-four male Sprague-Dawley rats, weighing 250-300 g, were unilaterally myringotomized and randomly separated into three groups. Group 1 received no treatment (control group) (n = 8); Group 2 received topical rosmarinic acid (n = 8); Group 3 received oral rosmarinic acid (n = 8). On the twenty-first day, the right ears were examined by otomicroscope and findings of myringosclerosis were recorded. Finally, all of the rats were euthanized and the tympanic membrane (TM) thickness and the severity of middle ear mucosal inflammation were evaluated histopathologically. Results: The myringosclerosis severity, TM thickness, and inflammation scores were found to be significantly higher in the control group than in the topical and systemic treatment groups (p < 0.05). There were no statistically significant differences in terms of TM thickness and inflammation scores between the topical and systemic treatment groups (p > 0.05). While moderate and severe myringosclerosis were higher in the control group, mild myringosclerosis was found to be higher in both treatment groups. Conclusion: The local and oral administration of rosmarinic acid suppressed inflammation, reduced TM thickness, and prevented the development of myringosclerosis in myringotomized rats.

Caffeic acid phenethyl ester (CAPE) is an active component of propolis produced by honey bees. Antioxidant and antiinflammatory properties of this compound have been shown with various studies. Because of these features CAPE has been a popular investigational agent in recent years. It is a promising treatment option, especially for the treatment of disorders related to inflammation and increased production of free oxygen radicals, such as tympanosclerosis. © 2018 Elsevier Inc. All rights reserved.

WOS: 000345108400003 Objective: The effects of serotonin and/or noradrenaline re-uptake inhibitors on memory have been investigated in various clinical and pre-clinical studies. However, contradictory results have been reported. In this study, the effect of the selective noradrenaline re-uptake inhibitors atomoxetine and reboxetine, a tricyclic antidepressant, amitriptyline, and a selective serotonin re-uptake inhibitor, paroxetine, on learning and memory were examined alone or in combination with scopolamine in mice using a passive avoidance task. Methods: Male Balb-C mice (25-30 g) were used. Reboxetine (10 mg/kg), atomoxetine (5 mg/kg), paroxetine (10 mg/kg) and amitriptyline (10 mg/kg) were investigated alone or in combination with scopolamine (1 mg/kg). A passive avoidance task was used to evaluate memory function. Acquisition time was recorded on the first day and retention time on the second (after 24 h). All drugs and saline were administered intraperitoneally 30 min prior to testing in order to evaluate retention time. Results: None of the drugs or saline impaired retention time when administered alone; however, scopolamine significantly impaired retention time (p=0.003). Reboxetine, atomoxetine and paroxetine all resulted in a marked improvement in retention time in combination with scopolamine. A combination of amitriptyline and scopolamine also significantly reduced retention time (p=0.013). Conclusion: Our results suggest that the effect of atomoxetine and reboxetine on improving memory deficit may be attributed to their inhibition of noradrenaline re-uptake. The effect of paroxetine on improving memory deficit may arise from enhanced serotonergic activity. Amitriptyline's lack of positive effect on memory deficit may be due to its own anticholinergic effect. Further studies using the same models and animal species are needed to clarify the mechanisms of the effects of each drug.

Objectives. We aimed to investigate the effect of a carbohydrate-rich diet on detrusor contractility in rats. Materials and Methods. Sprague-Dawley rats were randomized into two groups. The control group received regular food and water. The study group received carbohydrate-rich diet for six weeks. The rats’ detrusor muscle was isolated for pharmacological and histopathological examinations. Results. In the control and study groups, mean body weights were 431.5 ± 27.6 g and 528.0 ± 36.2 g, respectively (p < 0.001). Electrical stimulation of the detrusor strips of the control group resulted in gradual contraction. A decreased contractile response was shown in the study group. Acetylcholine in 10-7-10-3 molar concentration produced a decreased contractile response in the study group, compared to the control group (p < 0.01). The study group showed marked subepithelial and intermuscular fibrosis in the bladder. Conclusion. Carbohydrate-rich diet causes marked subepithelial and extracellular fibrosis and changes in contractility in the detrusor within a six-week period. Changes have higher costs in therapeutic choices and correction of these changes remains difficult. Putting an end to carbohydrate-rich diet would seem to be more cost-effective than dealing with the effects of consuming it in high proportions which should be the national policy worldwide.

Objective: We aimed to investigate the effects of a Carbohydrate-rich diet on vas deferens contractility and histology. Materials and Methods: Twenty mature male rats were subjected into two groups. The control group received regular food and water and the study group received regular food and a carbohydrate-rich liquid diet mixture of 37–40% fructose, 30–36% sucrose and 27–30% glucose instead of water and prepared stock diet was diluted with 50% water. Animals were weighted and sacrificed after six weeks and the vas deferens has been evaluated with in vitro studies. Five rats from both the control and study groups, were separated into subgroups for dapoxetine administration 4 hours before they were sacrificed. Results: At the beginning of this study, the mean body weights were 228.6±6.7 g (range: 205-237) and 231.4±9.6 g (range: 202-243) in control and study groups, respectively. The mean body weights were 247.1±4.8 g (236-252) in the control group and 318.8±9.3 g (314-326) in the study group ( p 0.05). Responses to Adenosine Three Phosphate (ATP) were also not significant ( p >0.05). The contractile responses at the same frequencies of electrical field stimulation (EFS) were similar in both groups ( p >0.05). Histological examinations showed no abnormalities in either group. Conclusion: Carbohydrate-rich diet caused no increase in fibrotic activity, and pharmacological and histological properties remained stable, but caused significant weight gain over a short time period. Furthermore, dapoxetine had no effect on the contractility of the vas deferens.

Bozkurt, Ayhan/0000-0002-5794-709X; Bilge, S.Sirri/0000-0003-2878-6968 WOS: 000373479600008 PubMed: 27114637 Objectives: To investigate nonsteroidal anti-inflammatory drugs effectiveness in colorectal distension (CRD)-induced visceral pain model. Materials and Methods: Male Sprague-Dawley (250-300 g) rats were anesthetized with ketamine (50 mg/kg, intraperitoneally [i.p.]) and chlorpromazine (25 mg/kg, i.p.). Two bipolar Teflon-coated Ni/Cr wire electrodes (80-M diameter) were placed in the abdominal external oblique muscle for the recording of electromyography. Jugular vein catheter was placed for the administration of drugs. CRD method was applied to evaluate of visceral pain. All drugs (paracetamol, meloxicam, metamizole, and dexketoprofen) administered intravenously. Results: Paracetamol 200, 400, and 600 mg/kg did not change the visceromotor response (VMR) when compare with the control group. Meloxicam 2 and 4 mg/kg showed no effect but at doses of 6 mg/kg meloxicam significantly ([51.9 +/- 6.4%] [P < 0.001]) decreased VMR compared with the control group. Metamizole 200 mg/kg did not change responses but dose of 400 and 600 mg/kg metamizole reduced VMR. Dexketoprofen 2 and 4 mg/kg did not cause a change in VMR but 6 mg/kg dose significantly reduced response compared with the control group ([43.9 +/- 3.9%, 36.8 +/- 2.8%, 34.8 +/- 2.5%, 42.1 +/- 4.8%, 40.7 +/- 3.5%, 36.4 +/- 2.7%, and 26.1 +/- 2.2%]; from 10 min to 70 min, respectively, [P < 0.05]). Conclusion: Metamizole, dexketoprofen and meloxicam show antinociceptive effect with different duration of action on CRD-induced visceral pain model. This condition can be explained due to different chemical structures and different mechanisms which play a role in modulation of pain. Ondokuz Mayis University Research FundOndokuz Mayis University [PYO.TIP. 1904.11.024] Ondokuz Mayis University Research Fund, PYO.TIP. 1904.11.024.

Balci, Hakan/0000-0003-4106-3211; WOS: 000358578400001 PubMed: 25394903 Agomelatine is a potent agonist at melatonergic 1 and 2 (MT1 and MT2) receptors and an antagonist at serotonin-2C (5HT-2C) receptors. It was suggested that psychotropic effects of agomelatine is associated with its melatonergic and serotonergic effects. In this study, we aimed to evaluate the effects of agomelatine alone or in combination with ritanserin (5HT-2A/2C antagonist) on memory and learning. Male Balb-C mice (25-30 g) were used, and all drugs and saline were administrated by intraperitoneal (i.p.) route 30 min prior to evaluating retention time. Whilst agomelatine was administered at the doses of 1, 10 and 30 mg/kg, ritanserin was administered at the doses of 0.1, 1 and 10 mg/kg. To evaluate memory function, passive avoidance test was used. On the first day, acquisition time and on the second day (after 24h), retention time of mice were recorded. To evaluate the synergistic activity, only the least doses of agomelatine and ritanserine were used, that is, 1 and 0.1 mg/kg, respectively. Scopolamine (1 mg/kg) was used as a reference drug, so it was combined with drug groups. Our results show that 5HT-2A/2C receptor antagonist ritanserin (1 and 4 mg/kg, i.p.) and agomelatine (10 and 30 mg/kg, i.p.) improve memory deficit induced by scopolamine, whilst a synergistic interaction is observed between ritanserin and agomelatine (0.1 mg/kg and 1 mg/kg, i.p., respectively) when they were administered at their ineffective doses. According to our findings, we concluded that agomelatine improves memory deficit and thus improves the effect of agomelatine arises from its 5HT-2C receptor antagonist activity.