Erbaş Oytun, Akseki Hüseyin Serdar, Solmaz Volkan, Aktuğ Hüseyin, Taşkıran Dilek
Department of Physiology, Faculty of Medicine, Gaziosmanpaşa University, Tokat, Turkey.
Department of Psychiatry, Tavşanlı State Hospital, Kütahya, Turkey.
Kaohsiung J Med Sci. 2014 Sep;30(9):447-52. doi: 10.1016/j.kjms.2014.05.007. Epub 2014 Jun 25.
Although understanding the relation between psychotic behavior and immune abnormalities has been the focus of research for many years, it remains to be elucidated whether the changes in cytokine levels are part of etiology or a result of the stress associated with the disorder. In accordance with previous studies on changes in cytokine levels due to metabolic changes and psychosis, we hypothesized that fatty liver may potentiate apomorphine-induced stereotypy in a rodent model and that a synthetic glucagon-like peptide-1 analog exenatide would ameliorate this effect. In this study, 18 male Sprague Dawley albino mature rats were used. We induced hepatosteatosis in these rats by feeding them with 30% fructose dissolved in drinking water for 8 weeks. The animals were divided into three groups, namely, the normal group, the intracerebroventricular (ICV) exenatide group, and the ICV NaCl group. Apomorphine-induced stereotypic behavior test was performed in all groups and the liver was removed for histopathological examination after all the rats were euthanized. In the nonalcoholic fatty liver (NAFL) group, stereotypy scores were significantly increased compared with the control group rats (p < 0.00001). A significant decrease in stereotypy scores were observed in the ICV exenatide group with NAFL when compared with the ICV saline group with NAFL (p < 0.005). In addition, brain malondialdehyde and tumor necrosis factor-α levels decreased in the ICV exenatide group. The results of this study showed that fatty liver enhances the effect of apomorphine on stereotypy, which was reversed by exenatide possibly by antioxidant and anti-inflammatory effects.
尽管多年来了解精神病行为与免疫异常之间的关系一直是研究的重点,但细胞因子水平的变化是病因的一部分还是该疾病相关应激的结果仍有待阐明。根据先前关于代谢变化和精神病导致细胞因子水平变化的研究,我们假设在啮齿动物模型中脂肪肝可能会增强阿扑吗啡诱导的刻板行为,并且一种合成的胰高血糖素样肽-1类似物艾塞那肽会改善这种效应。在本研究中,使用了18只雄性斯普拉格-道利白化成熟大鼠。通过给这些大鼠饮用溶解有30%果糖的水8周来诱导肝脂肪变性。将动物分为三组,即正常组、脑室内(ICV)注射艾塞那肽组和ICV注射氯化钠组。对所有组进行阿扑吗啡诱导的刻板行为测试,在所有大鼠安乐死后取出肝脏进行组织病理学检查。在非酒精性脂肪肝(NAFL)组中,与对照组大鼠相比,刻板行为评分显著增加(p < 0.00001)。与NAFL的ICV生理盐水组相比,NAFL的ICV艾塞那肽组的刻板行为评分显著降低(p < 0.005)。此外,ICV艾塞那肽组的脑丙二醛和肿瘤坏死因子-α水平降低。本研究结果表明,脂肪肝增强了阿扑吗啡对刻板行为的影响,而艾塞那肽可能通过抗氧化和抗炎作用逆转了这种影响。