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Intracerebroventricular injection of streptozotocin in rats produces both oxidative stress in the brain and cognitive impairment.

机译:大鼠脑室内注射链脲佐菌素会产生脑部氧化应激和认知障碍。

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Recent reports suggest the involvement of free radicals in the pathophysiology of Alzheimer's disease [AD]. Streptozotocin [STZ] injection in the brain is known to cause cognitive impairment in rats and is likened to sporadic AD in humans. Though STZ is known to cause impairment in glucose and energy metabolism, it is not known whether this is associated with free radical generation. The present study was designed to investigate if the changes in learning and memory by intracerebroventricular administration of STZ are associated with changes in the markers of oxidative stress. Adult male Wistar rats [330-340 g] were injected with intracerebroventricular STZ [3 mg/kg] bilaterally stereotaxically under ketamine anesthesia [70 mg/kg]. The rats were treated with STZ twice, on day 1 and on day 3. The learning and memory behavior was analyzed using passive avoidance paradigms, elevated plus maze and the closed field activity test while the parameters of oxidative stress assessed were malondialdehyde [MDA] and glutathione. The behavioral tests were performed on day 17, 18 and 19. The rats developed significant deficits in learning, memory and cognitive behavior, indicated by deficits in passive avoidance paradigm and elevated plus maze as compared to sham rats. On day 21, the rats were sacrificed under ether anesthesia and the brains were analyzed for biochemical studies. There was a development of oxidative stress in the brain as indicated by significant elevations in malondialdehyde [MDA] levels and decreased levels of glutathione. The study demonstrates that intracerebroventricular STZ may be appropriate model for investigations of antioxidants as potential treatment in Alzheimer's dementia.
机译:最近的报道表明自由基参与了阿尔茨海默氏病[AD]的病理生理。已知在大脑中注射链脲佐菌素(STZ)会导致大鼠认知功能障碍,并且可以将其与人的偶发性AD相提并论。尽管已知STZ会导致葡萄糖和能量代谢受损,但尚不清楚这是否与自由基生成有关。本研究旨在研究STZ的脑室内给药对学习和记忆的改变是否与氧化应激标志物的改变有关。成年雄性Wistar大鼠(330-340 g)在氯胺酮麻醉下(70 mg / kg)双侧立体定向注射脑室内STZ [3 mg / kg]。在第1天和第3天用STZ治疗大鼠两次。使用被动回避范例,高架迷宫和封闭田间活性测试分析学习和记忆行为,同时评估氧化应激参数为丙二醛[MDA]和谷胱甘肽。在第17、18和19天进行了行为测试。与假大鼠相比,大鼠在学习,记忆和认知行为上出现了明显的缺陷,这表现为被动回避范式的缺陷和加高迷宫的缺陷。在第21天,在乙醚麻醉下处死大鼠,并分析脑以进行生化研究。丙二醛(MDA)含量显着升高和谷胱甘肽水平降低表明大脑中存在氧化应激。这项研究表明,脑室内STZ可能是研究抗氧化剂作为阿尔茨海默氏痴呆症潜在治疗方法的合适模型。

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