Ozer Ciüdem, Gönül Bilge, Elmas Ciüdem, Erdoüan Deniz, Ercan Z Sevim
Faculty of Medicine, Department of Physiology, University of Gazi, Ankara, Turkey.
Mol Cell Biochem. 2005 Dec;280(1-2):151-7. doi: 10.1007/s11010-005-8842-7.
Dexfenfluramine is one of the anorectic drugs that suppresses food intake which acts via inhibition of reuptake of serotonin into brain terminal. Gastrointestinal tract is the main source of peripheral serotonin which is involved in the regulation of gastrointestinal motility. During the use of anorectic drugs, the antioxidant defence is affected especially by reactive oxygen species. The purpose of this study to search: The effect of dexfenfluramine on serotonin levels of ileum and the effect of dexfenfluramine on ileal contractility and oxidative stress.
Twenty-two adult male Swiss-albino mice were divided two groups (1) Control, (2) Dexfenfluramine treated (i.p. twice a day 0.2 mg kg(-1) in 0.2 ml saline solution for 7 days). Animal body weights were recorded at the beginning and at the end of the experimental period. Ileum tissues contractile responses to different concentrations of KCl and acethycholine were recorded on polygraph. In the meantime ileal tissue malondialdehyde, a product of lipid peroxidation, and glutathione, endogenous antioxidant levels were assessed by spectrophotometric methods. Ileal tissue serotonin level determined by immunohistochemical method. Body weights decrease and ileal contractile response of acethycholine increased significantly by dexfenfluramine treatment. Meanwhile, ileum glutathione levels decreased and malondialdehyde levels increased in dexfenfluramine treated group. Immunohistochemical detection showed that ileal serotonin levels increased by dexfenfluramine treatments. As a conclusion, there is a relationship between increased ileal contractility and oxidant status in dexfenfluramine treated animals. These effects can be related by increased serotonin levels which is induced by dexfenfluramine in ileum.
右芬氟拉明是一种通过抑制血清素再摄取进入脑终末来抑制食物摄入的食欲抑制药物。胃肠道是外周血清素的主要来源,其参与胃肠蠕动的调节。在使用食欲抑制药物期间,抗氧化防御尤其受到活性氧的影响。本研究的目的是探究:右芬氟拉明对回肠血清素水平的影响以及右芬氟拉明对回肠收缩性和氧化应激的影响。
22只成年雄性瑞士白化小鼠分为两组:(1)对照组;(2)右芬氟拉明处理组(每天腹腔注射两次,每次0.2 mg/kg,溶于0.2 ml盐溶液中,共7天)。在实验期开始和结束时记录动物体重。在多道生理记录仪上记录回肠组织对不同浓度氯化钾和乙酰胆碱的收缩反应。同时,通过分光光度法评估回肠组织中脂质过氧化产物丙二醛和内源性抗氧化剂谷胱甘肽的水平。通过免疫组织化学方法测定回肠组织血清素水平。右芬氟拉明处理导致体重下降,乙酰胆碱引起的回肠收缩反应显著增加。同时,右芬氟拉明处理组回肠谷胱甘肽水平降低,丙二醛水平升高。免疫组织化学检测显示,右芬氟拉明处理使回肠血清素水平升高。结论是,在右芬氟拉明处理的动物中,回肠收缩性增加与氧化状态之间存在关联。这些影响可能与右芬氟拉明诱导回肠血清素水平升高有关。