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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]

Copyright of Journal of Anatolia Nursing & Health Sciences / Anadolu Hemsirelik Ve Saglik Bilimleri Dergisi is the property of Ataturk University Coordinatorship of Scientific Journals and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Turkish Journal of Oncology / Türk Onkoloji Dergisi is the property of KARE Publishing and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

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]

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-α, IL-1β 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-α, IL-1β, 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-α, IL 1-β, 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]

Copyright of Mediterranean Journal of Infection, Microbes & Antimicrobials is the property of Galenos Yayinevi Tic. LTD. STI and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

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]

Copyright of Marmara Medical Journal is the property of Marmara Medical Journal and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Turkish Journal of Biochemistry / Turk Biyokimya Dergisi is the property of De Gruyter and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of RAED Journal / RAED Dergisi is the property of Deomed Publishing and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)