3 research outputs found

    Effect of Garcinia cambogia Extract on Fatty Liver in Rats Fed High Lipid

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    Garcinia cambogia is a plant which contains hydroxycitric acid and suppresses appetite and body fat accumulation. The aim of the study was to investigate the improving effect of Garcinia cambogia-extract on liver phospholipid, triglyceride, lipid hydroperoxide, total protein and gamma-glutamyltransferase (GGT) activity, and histopathology of liver in female rats fed high-lipid diet. One-year-old 30 female Sprague-Dawley rats were separated to three equal groups. Group 1 (control group) was fed basal diet (2% liquid vegetable oil, 0% cholesterol), while the diets of both group 2 and 3 contained vegetable oil (2% liquid and 5% hydrogenated vegetable oil) and cholesterol (3%). 4.5% (W/W) Garcinia cambogia-extract was added to the diet of group 3 from day 45. Rats were euthanized on day 75. Liver samples were weighed, homogenized and centrifuged to obtain post-mitochondrial fractions (PMF). PMF phospholipid levels significantly decreased in the group fed high-lipid diet compared with the control group and in the group fed Garcinia cambogia-extract compared with the other two groups (P<0.05). PMF lipid hydroperoxide levels were significantly higher and PMF triglyceride levels were significantly lower in the control group than those in the other two groups (P<0.05). In the result of histopathological examinations, marked fat infiltration was observed in hepatocytes of animals fed high-lipid diet. Livers of animals fed Garcinia cambogia-added diet showed moderate fat infiltrations of the hepatocytes. Liver fattening partly occurred in rats fed high-lipid diet. However, this did not lead to the severe cellular degeneration. Garcinia cambogia added to the high-lipid diet insufficiently impaired liver fattening in the present dose

    Evaluation of Bcl-2, Bcl-X-L and Bax Expression and Apoptotic Index in Canine Mammary Tumours

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    Mammary tumours are the most common neoplasms in intact female dogs. Dysregulation of programmed cell death mechanisms plays an important role in the pathogenesis and progression of mammary gland tumours. The aim of this study was to investigate the relationship between some anti-apoptotic proteins (Bcl-2, Bcl-X-L and Bax), apoptotic index (AI) and histopathological diagnosis, tumour grading, tumour staging and survival time of canine mammary tumours (CMT). Twenty seven tissue samples were collected from twenty seven animals with mammary tumours. The samples were evaluated and graded histopathologically. All cases were staged according to the TNM system. The expression of Bcl-2, Bcl-X-L and Bax proteins was investigated using indirect immunoperoxidase test and apoptosis was evaluated using terminal deoxynucleotidyltransferase (TdT)-mediated nick end-labelling (TUNEL) technique. Follow-up examination and survival estimation analysis were performed. While there was a significant statistical relation between Bcl-2 expression and histopathological diagnosis (P0.05). The differences between T1 and T5, T2 and T5 stages were statistically significant in terms of Bax expression (P0.05). Bcl-2 was overexpressed in highly malignant tumours such as solid and tubulopapillary adenocarcinomas and Bax had high expression levels in metastatic tumours. As a result, it is concluded that Bcl-2 and Bax expression can be accessory parameters for anticipating the biologic behaviour and prognosis of CMT but these markers alone are not sufficient for the determination of survival time

    Aggravating effect of atorvastatin on indomethacin-induced gastric injury: Focus on PGE(2), TNF-alpha, neutrophils and iNOS

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    Statins are suggested to possess healing properties due to their antioxidant and antiinflammatory effects in animal ulcer models. In contrary, a clinical report indicated the formation of gastric ulcer by the use of atorvastatin. In this study, we aimed to investigate the effects of atorvastatin (0.5, 5 and 50 mg/kg, p.o.) after single (acute) and multiple (subchronic, 5 days) applications on indomethacin-induced gastric ulcer in rats. In both acute and subchronic models high dose atorvastatin (50 mg/kg), unlike to lower doses (0,5 and 5 mg/kg), significantly aggravated ulcer lesions induced by indomethacin (30 mg/kg) although, a direct ulcerogenic influence was lacking. Proulcerogenic effect of atorvastatin are likely to be associated with decreased mucosal defense mechanisms (GSH and PGE(2)), and increased neutrophil infiltration and proinflammatory factors (TNF-a and iNOS) possibly via independently from mevalonate pathway. Thus, atorvastatin therapy should be monitorized in patients for an increased risk of gastric ulcer particularly when used concomitantly with NSAIDs. (c) 2015 Published by Elsevier Inc
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