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Riparin II ameliorates corticosterone-induced depressive-like behavior in mice: Role of antioxidant and neurotrophic mechanisms
Neurochemistry international ( IF 4.2 ) Pub Date : 2018-07-21 , DOI: 10.1016/j.neuint.2018.07.007
Iardja Stéfane Lopes , Iris Cristina Maia Oliveira , Victor Celso Cavalcanti Capibaribe , José Tiago Valentim , Daniel Moreira Alves da Silva , Alana Gomes de Souza , Mariana Albuquerque de Araújo , Raquell de Castro Chaves , Stanley Juan Chaves Gutierrez , José Maria Barbosa Filho , Danielle Silveira Macêdo , Francisca Cléa Florenço de Sousa

Riparin II (RIP II) is an alkamide isolated from Aniba riparia that has presented antidepressant and anxiolytic effects in acute stress behavioral models. This study aimed to investigate the activity of RIP II in a corticosterone-induced depression mice model. Corticosterone (20 mg/kg, s.c.) was administered once a day for 21 days. RIP II (50 mg/kg, p.o.) or fluvoxamine (FLU, 50 mg/kg, standard antidepressant, p.o.) was administered after corticosterone (CORT) injection, for the last 7 days of CORT treatment. Mice were exposed to the following behavioral tests: forced swimming, tail suspension, open field, sucrose preference, elevated plus maze and ymaze. After behavioral evaluation, brain areas (prefrontal cortex, hippocampus and striatum) were dissected for neurochemical evaluation: oxidative stress parameters (MDA, nitrite and GSH) and BDNF dosage. Repeated CORT administration caused depressive-like behavior in mice as indicated by increased despair effects in forced swimming and tail suspension tests and anhedonia in sucrose preference test. In addition, CORT decreased BDNF levels in the mice hippocampus and induced oxidative load in the brain with significative increase in pro-oxidant markers (lipid peroxidation and nitrite levels) and a decline in anti-oxidant defense system (reduced glutathione levels), indicating a direct effect of stress hormones in the induction of the brain oxidative stress. On the other hand, RIP II treatment reversed CORT-induced depressive-like behavior. Furthermore, this treatment reversed the impairment in BDNF levels and oxidative brain insults caused by CORT. This may demonstrate the mechanisms involved in antidepressant-like effect of RIP II. These findings further support that RIP II may be implicated as pharmacological intervention targeting depression associated with HPA-axis dysregulation.



中文翻译:

Riparin II改善小鼠皮质酮诱导的抑郁样行为:抗氧化剂和神经营养机制的作用

Riparin II(RIP II)是一种分离自河滨Aniba riparia的链烷酰胺在急性应激行为模型中显示出抗抑郁和抗焦虑作用。这项研究旨在调查RIP II在皮质酮诱导的抑郁症小鼠模型中的活性。皮质酮(20 mg / kg,sc)每天给药一次,持续21天。皮质酮(CORT)注射后,在CORT治疗的最后7天中,服用RIP II(50 mg / kg,口服)或氟伏沙明(FLU,50 mg / kg,标准抗抑郁药,口服)。小鼠接受以下行为测试:强迫游泳,尾巴悬吊,空旷,蔗糖偏爱,高架迷宫和迷宫。进行行为评估后,解剖大脑区域(额叶皮层,海马和纹状体)以进行神经化学评估:氧化应激参数(MDA,亚硝酸盐和GSH)和BDNF剂量。反复进行CORT给药会在小鼠中引起抑郁样行为,如强迫游泳和尾巴悬吊测试中绝望效应的增加以及蔗糖偏爱测试中的快感缺乏症所表明的那样。此外,CORT降低了小鼠海马中的BDNF水平,并诱导了大脑中的氧化负荷,促氧化剂标志物(脂质过氧化和亚硝酸盐水平)显着增加,抗氧化防御系统下降(谷胱甘肽水平降低),表明应激激素在诱导脑部氧化应激中的直接作用。另一方面,RIP II治疗可逆转CORT诱导的抑郁样行为。此外,这种治疗可以逆转由CORT引起的BDNF水平受损和氧化性脑损伤。这可能证明了与RIP II的抗抑郁样作用有关的机制。

更新日期:2018-07-21
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