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Objective: 5-Fluorouracil (5-FU), a widely administered anti-cancer drug, causes gastrointestinal damage through various mechanisms. This study aimed to investigate the ameliorative effect of silk fibroin (SF), which has anti-inflammatory and antioxidant properties, against 5 FU-induced gastrointestinal damage. Materials and methods: Wistar albino rats were divided into 3 groups; Control group, 5-FU group (30mg/kg/day on days 0, 2, 4), and 5-FU+SF (30 mg/kg/day 5-FU on days 0, 2, 4 + 600 mg/kg/day SF for 14 days). At the end of the experiment, stomach and intestinal tissue samples were collected and immunohistochemically iNOS, caspase-3, CD4+ and CD8+ were measured. Besides, structural damage was assessed with hematoxylin-eosin and caspase-3 and 9 activities were evaluated using western blot analysis. Results and Discussion: It was determined that iNOS, caspase-3, caspase-9 activities, CD4+ and CD8+ levels and structural damage significantly increased in both stomach and intestinal tissues. Furthermore, elevated markers were regressed almost to control levels in SF administrated group. Conclusion: SF may have an ameliorative effect, thus reducing the gastrointestinal damage caused by 5 FU. More clinical and scientific research should be conducted as the silk fibroin may be a suitable candidate against the adverse effects of chemotherapeuic agents. [ABSTRACT FROM AUTHOR]

The incidence of Brucella canis (B. canis) in humans is unknown in Northern Cyprus. In this study, we investigated the prevalence of B. canis and Brucella abortus (B. abortus) infection in human sera and evaluated the results obtained by agglutination-based techniques using standardized antigens made from B. canis comparatively. All of the subjects were negative in terms of Rose-Bengal plate test. Undiluted serum samples were initially screened by rapid slide agglutination test (RSAT), and those which were found positive were retested in the dilution of 1/25-1/200. Confirmation of the positive results was performed by using 2-mercaptoethanol standard agglutination test (SAT). The test antigen was prepared from the less mucoid M (-) variant of B. canis, and 1/1,048 titered dog antiserum was used as positive control. In 225 serum samples, 3.6% (8/225) was positive by B. canis M (-) RSAT, 4.4 % (10/225) was positive by B. canis M (-) indirect enzyme-linked immunosorbent assay (iELISA). 5.3% (12/225) was positive by B. abortus S99 RSAT and 9.8% (22/225) was positive by B. abortus S99 iELISA. Nine samples were positive by both B. abortus S99 RSAT and B. abortus S99 iELISA. Seven samples were positive by both B. canis M (-) RSAT and B. canis M (-) iELISA. One patient was positive by all methods. It is important to evaluate patient samples with RSAT and iELISA. Until the notification system gives better results to the Ministry of Health, in order to reach the real data for Northern Cyprus, multicenter prevalence determination studies should be done for future. [ABSTRACT FROM AUTHOR]

Introduction: We examined the effects of chitosan (CTS) for reducing cisplatin (CIS)-induced hepatorenal toxicity in a rat model. Methods: A hepatorenal toxicity model was established by administering a single dose of 7 mg/kg CIS intraperitoneally (i.p) to Wistar albino rats. After seven days of once-daily normal saline or CTS (200 mg/kg; po) treatment, liver and kidney tissue samples were obtained from rats and Bcl-2/Bax ratio and caspase-3 expression levels were evaluated by Western blotting method. Histologically, structural damage was measured under a light microscope, and the degree of damage to organs was evaluated by a scoring system. Results: CIS-induced hepatorenal damage was reversed with CTS treatment in the renal and hepatic tissues (p<0.05). Overall, CISinduced increases in apoptotic parameters, Bcl-2/Bax ratio and caspase-3 expression, were reversed by CTS treatment (p<0.05). Conclusion: It was determined that CTS, a biopolymer, may have a protective effect by preventing hepatorenal damage caused by CIS. [ABSTRACT FROM AUTHOR]

Objectives: The purpose of this study was to investigate possible protective effects of St. John's wort in the hepatic ischemia/reperfusion injury. Material and Methods: The hepatic artery, portal vein, and bile duct were all clamped for 45 minutes to induce ischemia in rats, and after that reperfusion for 1 hour. SJW was administrated orally, once a day for 3 days before ischemia/reperfusion. The aspartate aminotransferase, alanine aminotransferase, tumor necrosis factor, and interleukin levels were measured in the serum samples. Luminol chemiluminescence, lucigenin luminol chemiluminescence levels; myeloperoxidase. The sodium-potassium ATPase (Na+/K+ ATPase) activity was determined in the liver tissue, and caspase-3 and caspase-9 activity with the bcl-2/bax ratio were measured by the western blot analysis. Results: The St. John's wort administration recovered the aspartate aminotransferase, alanine aminotransferase, tumor necrosis factor, and IL-1ß levels serum parameters meaningfully, while ischemia/reperfusion caused an increase in luminol chemiluminescence, lucigenin luminol chemiluminescence, myeloperoxidase, caspase-3, and caspase-9 activity and led to a decrease in the B-cell lymphoma-2/bcl-2-associated X protein (bcl-2/bax) ratio and the Na+/K+ ATPase activity. Conclusion: The obtained results indicate protective effects of St. John's wort on the ischemia/reperfusion injury through various mechanisms, and we are able to suggest that St. John's wort can clinically create a new therapeutic principle. [ABSTRACT FROM AUTHOR]

We compared different stress conditions on brain BDNF levels, in rats exposed to social isolation test (SIT) and predator scent tests (PST). BDNF expression in the frontal cortex, hippocampus, and amygdala was compared, and effects of chronic fluoxetine (FLU) treatment were evaluated. Rats were exposed to SIT and PST for one month. FLU was given (5 mg/kg/day, ip) throughout stress procedures. Controls, stress, and treatment groups were evaluated in elevated plus maze, anxiety scores were calculated. BDNF expression was determined by Western blot. SIT and PST induced anxiety in both sexes, females had greater anxiety scores than males (p<0.05). FLU restored anxiety scores in both sexes (p<0.01) in both tests. Male and female rats exhibited reduced cortical BDNF levels in SIT (p<0.001). PST reduced cortical BDNF in females, but increased in males. Hippocampal BDNF expression was lowered in SIT (p<0.01) and PST (p<0.001) in both sexes. Female rats had 40% lower BDNF expression than males in the amygdala in SIT. FLU did not restore cortical BDNF in females in both tests, but reduced increased BDNF levels in males in PST (p<0.001). FLU did not restore reduced brain BDNF in males in the hippocampus and amygdala, but restored in hippocampus, in females. Our findings indicate that sex differences must be considered in studies related to mood disorders of animal models, and suggest that BDNF expression in different brain regions are altered differentially in a gender-dependent manner in rats. Antianxiety effect of FLU is not mediated through increasing BDNF activity in cortex in both genders. Increased BDNF in hippocampus and amygdala may reflect antidepressant effect of FLU in female rats, but not in males. [ABSTRACT FROM AUTHOR]

Ulcers that develop due to alcohol consumption are frequently confronted. The aim of this study was to investigate the protective effects of silk fibroin on the pro-apoptotic and anti-apoptotic protein expression levels on ethanol induced-ulcer models in rats. For three consecutive days, orogastrically either silk fibroin or saline were given to rats. On the 4th day, animals were deprived of food but allowed free access to water for 24 h before the experiment. While control groups were treated with only physiological saline, the ulcer groups were treated orally either with saline or silk fibroin groups. For ulcer induction, 1 ml of absolute ethanol by gavage were given to both group. Firstly, intracardiac blood was taken at 60 min of EtOH or saline administration and immediately animals were decapitated. In blood samples, the amount of TNF-, IL-1ß were analysed whereas in stomach tissues, the levels of MDA, GSH, and MPO activity and the expression levels of bcl-2, Bax, caspase-3 and -9 were determined. In ulcer groups, the amount of TNF-, IL-1ß, MDA, MPO, caspase-3 and caspase-9 were found to be significantly higher compared to control groups whereas in GSH, Bcl-2/Bax were found to be lower (p < 0.005). In treatment groups it is observed that silk fibroin recovers the amount of TNF-, IL 1-ß, MDA, MPO, GSH, caspase-3, caspase-9, and Bcl- 2/Bax. In conclusion, for the treatment of the gastric ulcer SF thought to be very efficient therapeutic agent. [ABSTRACT FROM AUTHOR]

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BACKGROUND: This study was designed to determine possible protective effect of betaine treatment against oxidative injury in pulmonary tissue induced with thermal trauma. METHODS: Under ether anesthesia, shaved dorsum of Wistar albino rats was exposed to a 90°C water bath for 10 seconds to induce burn injury. Betaine was administered orally (250 mg/kg) for a period of 21 days before burn injury, and single dose of betaine was administered after thermal injury. Control group rats were exposed to 25°C water bath for 10 seconds. Upon conclusion of experiment, rats were decapitated and blood was collected for analysis of pro-inflammatory cytokines and lactate dehydrogenase (LDH) activity. Lung tissue samples were taken to determine malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO), and Na+K+-ATPase activity, in addition to histological analysis. RESULTS: Burn injury caused significant increase in both cytokine levels and LDH activity. In lung samples, raised MDA levels, MPO activity, and reduced GSH levels and Na+/K+-ATPase activity were found due to burn injury. CONCLUSION: Treatment of rats with betaine significantly restored GSH level and Na+K+-ATPase activity, and decreased MDA level and MPO activity. According to the findings of the present study, betaine significantly diminishes burn-induced damage in tissue. [ABSTRACT FROM AUTHOR]

Objectives: Activation of neuronal nitric oxide synthase (nNOS) and interrelated alterations of calmodulin and ionotropic glutamate receptor (GluN1) levels are unknown in post traumatic stress disorder (PTSD). Materials and Methods: Sprague-Dawley rats of both sexes were exposed to dirty cat litter, and then placed on an elevated plus maze. An anxiety index was calculated and tissue samples from hippocampus and amygdala were prepared in order to detect calmodulin, NOS and GluN1 by immunoblotting. Results: The anxiety indices of the traumatized rats were markedly higher than those of the controls (p<0.05). GluN1 and calmodulin levels were decreased in the dorsal hippocampus and amygdaloid complex of the traumatized rats. NOS expression increased significantly in both the amygdaloid complex and dorsal hippocampus where the increase was statistically more prominent in the amygdaloid complex (p< 0.001) than in the dorsal hippocampus of the traumatized rats (p<0.05). Conclusion: Predator exposure in rats causes long-lasting anxiogenic effects associated with increases in NOS and decreases in GluN1 expressions in brain areas related to PTSD symptoms and excitotoxicity. The results suggest that excitotoxicity occurs through other mechanisms rather than GluN1 receptors. [ABSTRACT FROM AUTHOR]

Objective: The B-cell lymphoma/leukemia-2 (Bcl-2) family of proteins governs mitochondrial membrane permeability where the programmed apoptotic process is controlled by the balance between proapoptotic (Bax) and antiapoptotic (Bcl-2) proteins. We aimed to investigate the [Bcl-2]/[Bax] in different brain regions in a post-traumatic stress disorder rat model. Methods: Female Sprague-Dawley rats were exposed to dirty cat litter (trauma) for 10 min and the protocol was repeated 1 week later with a trauma reminder (clean litter) in reversed 12 h light/dark cycle. The rats received intraperitoneal saline, fluoxetine (2.5 mg/kg/day) or propranolol (10 mg/kg/day) for 7 days between exposure sessions. Following exposure to the trauma reminder, elevated plus maze experiments were done. Immunoblotting was used to quantify [Bcl-2] and [Bax] proteins in the homogenates of the dorsal hippocampus, the frontal cortex and the amygdaloid complex. Results: Fluoxetine reversed the increases in the anxiety indices and the freezing times. In the amygdaloid complex and the frontal cortex, the [Bcl-2]/[Bax] decreased in the traumatized control rats significantly (p<0.0001), but not in the dorsal hippocampus. Although the fluoxetine treatment reversed the apoptotic changes but propranolol failed and caused proapoptotic proteins to increase. Conclusion: These results may suggest a neuroprotective role for fluoxetine but not for propranolol. [ABSTRACT FROM AUTHOR]

Background: This study was designed to determine possible protective effect of betaine treatment against oxidative injury in pulmonary tissue induced with thermal trauma., Methods: Under ether anesthesia, shaved dorsum of Wistar albino rats was exposed to a 90°C water bath for 10 seconds to induce burn injury. Betaine was administered orally (250 mg/kg) for a period of 21 days before burn injury, and single dose of betaine was administered after thermal injury. Control group rats were exposed to 25°C water bath for 10 seconds. Upon conclusion of experiment, rats were decapitated and blood was collected for analysis of pro-inflammatory cytokines and lactate dehydrogenase (LDH) activity. Lung tissue samples were taken to determine malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO), and Na+/K+-ATPase activity, in addition to histological analysis., Results: Burn injury caused significant increase in both cytokine levels and LDH activity. In lung samples, raised MDA levels, MPO activity, and reduced GSH levels and Na+/K+-ATPase activity were found due to burn injury., Conclusion: Treatment of rats with betaine significantly restored GSH level and Na+/K+-ATPase activity, and decreased MDA level and MPO activity. According to the findings of the present study, betaine significantly diminishes burn-induced damage in tissue.