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Öğe Chitosan and blueberry treatment induces arginase activity and inhibits nitric oxide production during acetaminophen-induced hepatotoxicity(Wolters Kluwer Medknow Publications, 2014) Özçelik, Eda; Uslu, Sema; Burukoğlu, Dilek; Musmul, AhmetBackground: Liver diseases have become a major problem of the worldwide. More than 50% of all cases of liver failure can be attributed to drugs. Among these, acetaminophen is the most common cause. Objective: The aim of this study was to investigate the the hepatoprotective effects of blueberry and chitosan on tissue arginase activity, ornithine and nitric oxide levels during the acetaminophen-induced hepatotoxicity. Materials and Methods: Acetaminophen (250 mg/kg body weight per day), blueberry (60 mg/kg body weight per day) and, chitosan (200 mg/kg body weight per day) were administered to the rats by oral gavage during the experimental period. Results: Blueberry and chitosan significantly decreased liver arginase activity and ornithine levelsand and increased nitric oxide levels. Glutathione levels were remarkably increased by chitosan and blueberry treatments. Conclusion: The results of the present study indicate that blueberry and chitosan effectively protected against the acetaminophen-induced hepatotoxicity. The hepatoprotective effect afforded by blueberry and chitosan can be attributed to its antioxidant and anti-inflammatory activities.Öğe Effect of hesperidin treatment on α-Klotho/FGF-23 pathway in rats with experimentally-induced diabetes(Elsevier Masson SAS, 2019) Dokumacıoğlu, Eda; İskender, Hatice; Musmul, AhmetObjective Non-alcoholic fatty liver disease, steatohepatitis and nephropathy are considered among the mostimportant complications of diabetes mellitus (DM), which recently increased due to increased frequency of DMand the prolonged life span of diabetic patients The aim of the present study was to reveal the possible effect ofhesperidin (HP) on alpha-klotho (?-KL)/fibroblast growth factor-23 (FGF-23) pathway in rats with diabetesinduced by streptozotocin (STZ).Materials and methods Thirty six male Sprague-Dawley rats were randomly divided into three groups. Therats of the control, diabetes, and treatment groups were fed with standard feed and water throughout the 2-weekstudy. In order to induce diabetes mellitus in rats, those in the diabetes group were administered a single dose of50 mg/kg STZ. For the DM + HP group, a single dose of 50 mg/kg STZ, when diabetes was induced, hesperidinwas administered orally at a dose of 100 mg/kg by gavage.Results The?-KL levels of our study groups, both the liver and kidney?-KL levels and serum?-KL of the STZ-induced diabetic group were statistically significantly lower than the control group (respectively, p < 0.05,p < 0.001, p < 0.05). It was observed that hesperidin administration statistically significantly increased?-KLlevels in serum, liver and renal tissue (p < 0.001). Liver, kidney and serum FGF-23 levels of the diabetic groupincreased significantly in comparison to the control group (respectively, p < 0.05, p < 0.01, p < 0.001). FGF-23 levels that increased in kidney tissue and serum samples of the diabetic group decreased statistically sig-nificantly with hesperidin administration (respectively, p < 0.01, p < 0.001).Conclusion The?-KL/FGF-23 pathway is a promising bio-indicator in various cases of systemic toxicity andpathology. In addition, the strong positive effects of hesperidin administration on diabetic toxicity in the liverand kidneys suggest that it may be included in the alternative treatment methods in the future.Öğe The effect of sulforaphane on oxidative stress and inflammation in rats with toxic hepatitis induced by acetaminophene(Comenius University, 2017) Dokumacıoğlu, Eda; İskender, Hatice; Aktaş, M. Sabih; Hanedan, Başak; Dokumacıoğlu, Ali; Şen, Tuğba Mazlum; Musmul, AhmetOBJECTIVE: The aim of the present study was to reveal the possible effect of sulforaphane on oxidative stress and inflammation in rats liver with toxic hepatitis induced by acetaminophene. BACKGROUND: Sulforaphane is a compound with high antioxidant properties. Acetaminophen, which is a para-aminophenol derivative, can lead to fatal hepatic necrosis with direct hepatotoxic effects at high doses. METHODS: Thirty six male Sprague-Dawley rats were randomly divided into four groups. Control group (n = 9) was fed with standard rat chow and water for 3 days. Group APAP (n = 9) received a single dose acetaminophen 1 g/kg by oral gavage in addition to standard chow and water. Group SFN (n = 9) received sulforaphane 500 mu g/kg by oral gavage in addition to standard chow and water for 3 days. Group APAP+SFN (n = 9) received sulforaphane 500 mu g/kg and a single dose acetaminophen 1 g/kg by oral gavage in addition to standard chow and water. Acetaminophen was administered three hours after SFN administration. RESULTS: Neopterin, MDA, AST, ALT and CRP levels of group APAP were significantly increased compared to control group. GSH level of group APAP was significantly lower than in the control group. CONCLUSION: Sulforaphane is a protective agent against acetaminophen-induced liver damage and it can be added in the treatment protocol (Tab. 1, Fig. 5, Ref. 51). Text in PDF www.elis.sk.Öğe Plasminogen activator inhibitor-1 and susceptibility to lung cancer: a population genetics perspective(Mary Ann Liebert Inc., 2014) Bayramoğlu, Ayşegül; Güneş, Hasan Veysi; Metintaş, Muzaffer; Degirmenci, İrfan; Güler, Halil İbrahim; Üstüner, Cengiz; Musmul, AhmetAim: The aim of this study was to investigate the polymorphism frequency of plasminogen activator inhibitor-1 (PAI-1) (rs1799889) 4G/5G in patients with lung cancer. Methods: In this study, 286 genomic DNAs (154 lung cancer patients + 132 subjects without lung cancer) were analyzed. Polymorphisms were determined by using the polymerase chain reaction (PCR) method, with 4G and 5G allele-specific primers. PCR products were assessed by a charge-coupled device camera and exposed to 2% agarose gel electrophoresis. Results: The frequencies of the PAI-1 gene 4G/5G genotypes were found to be 21% 4G/4G, 16% 4G/5G, and 62% 5G/5G in the control group and 31.4% 4G/4G, 30.8% 4G/5G, and 37.8% 5G/5G in the patient group. It was determined that the 5G/5G genotype frequency was high in patients in comparison with other genotypes. Conclusions: This study found a statistically significant difference between the groups with respect to genotype distribution. Consequently, we can say that the PAI-1 gene 4G/5G polymorphism is associated with lung cancer in Turkey.
