Debom Gabriela, Gazal Marta, Soares Mayara Sandrielly Pereira, do Couto Carlus Augustu Tavares, Mattos Bruna, Lencina Claiton, Kaster Manuella Pinto, Ghisleni Gabriele Codenonzi, Tavares Rejane, Braganhol Elizandra, Chaves Vitor Clasen, Reginatto Flávio Henrique, Stefanello Francieli, Spanevello Roselia Maria
Programa de Pós Graduação em Bioquímica e Bioprospecção, Laboratório de Neuroquímica, Inflamação e Câncer, Centro de Ciências Químicas, Farmacêuticas e de Alimentos, Universidade Federal de Pelotas, Campus Universitário S/N, Pelotas, RS, Brazil.
Programa de Pós Graduação em Biologia Celular e Molecular, Pontifícia Universidade Católica do Rio Grande do Sul, Porto Alegre, RS, Brazil.
Brain Res Bull. 2016 Oct;127:260-269. doi: 10.1016/j.brainresbull.2016.10.008. Epub 2016 Oct 18.
The aim of the present study was to evaluate the protective effects of blueberry extract on oxidative stress and inflammatory parameters in a model of mania induced by ketamine administration in rats. Male rats were pretreated with blueberry extract (200mg/kg, once a day for 14days), lithium chloride (45mg/kg, mood stabilizer used as a positive control, twice a day for 14days), or vehicle. Between the 8th and 14th days, rats also received an injection of ketamine (25mg/kg) or vehicle. In the 15th day, thirty minutes after ketamine administration the hyperlocomotion of the animals was assessed in the open - field apparatus. Immediately after the behavioral analysis brain and blood were collected for biochemical determinations. ketamine treatment induced hyperlocomotion and oxidative damage in cerebral cortex, hippocampus and striatum such as an increase in lipid peroxidation and a decrease in the antioxidant enzymes activities (superoxide dismutase, catalase e glutatione peroxidase). Ketamine administration also increased the IL-6 levels in serum in rats. Pretreatment of rats with blueberry extract or lithium prevented the hyperlocomotion, pro - oxidant effects and inflammation induced by ketamine. Our findings suggest that blueberry consumption has a neuroprotective potential against behavioral and biochemical dysfunctions induced in a preclinical model that mimic some aspects of the manic behavior.
本研究的目的是评估蓝莓提取物对氯胺酮诱导的大鼠躁狂模型中氧化应激和炎症参数的保护作用。雄性大鼠分别用蓝莓提取物(200mg/kg,每天一次,共14天)、氯化锂(45mg/kg,用作阳性对照的情绪稳定剂,每天两次,共14天)或赋形剂进行预处理。在第8天至第14天期间,大鼠还接受氯胺酮(25mg/kg)或赋形剂注射。在第15天,氯胺酮给药30分钟后,在旷场装置中评估动物的运动亢进情况。行为分析后立即采集大脑和血液进行生化测定。氯胺酮治疗诱导大脑皮质、海马和纹状体的运动亢进和氧化损伤,如脂质过氧化增加和抗氧化酶活性(超氧化物歧化酶、过氧化氢酶和谷胱甘肽过氧化物酶)降低。氯胺酮给药还增加了大鼠血清中的IL-6水平。用蓝莓提取物或锂对大鼠进行预处理可预防氯胺酮诱导的运动亢进、促氧化作用和炎症。我们的研究结果表明,食用蓝莓对在模拟躁狂行为某些方面的临床前模型中诱导的行为和生化功能障碍具有神经保护潜力。