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Amelioration of motor and non-motor deficits and increased striatal APoE levels highlight the beneficial role of pistachio supplementation in rotenone-induced rat model of PD.
Metabolic Brain Disease ( IF 3.2 ) Pub Date : 2020-06-11 , DOI: 10.1007/s11011-020-00584-5
Saida Haider 1 , Syeda Madiha 1 , Zehra Batool 2
Affiliation  

Pistachio contains polyphenolic compounds including flavonoids and anthocyanins which have antioxidant and antiinflammatory activity. Present study was aimed to evaluate the protective effects of pistachio on neurobehavioral and neurochemical changes in rats with Parkinson’s disease (PD). Animal model of PD was induced by the injection of rotenone (1.5 mg/kg/day, s.c.) for 8 days. Pistachio (800 mg/kg/day, p.o.) was given for two weeks in both pre- and post-treatment. At the end of treatment brain was dissected out and striatum was isolated for biochemical and neurochemical analysis. Memory was assessed by Morris water maze (MWM) and novel object recognition (NOR) test while open field test (OFT), Kondziela inverted screen test (KIST), pole test (PT), beam walking test (BWT), inclined plane test (IPT) and footprint (FP) test were used to observe motor behavior. Rotenone administration significantly (p < 0.01) impaired the memory but pistachio in both pre- and post-treatment groups significantly (p < 0.01) improved memory performance. Rotenone-induced motor deficits were significantly attenuated in both pre- and post-pistachio treatment. Increased oxidative stress and decreased DA and 5-HT levels induced by rotenone were also significantly attenuated by pistachio supplementation. Furthermore, raised apolipoprotein E (APoE) levels in rotenone injected rats were also normalized following treatment with pistachio. Present findings show that pistachio possesses neuroprotective effects and improves memory and motor deficits via increasing DA levels and improving oxidative status in brain.



中文翻译:

运动和非运动缺陷的改善和纹状体 APoE 水平的增加突出了开心果补充剂在鱼藤酮诱导的 PD 大鼠模型中的有益作用。

开心果含有多酚化合物,包括具有抗氧化和抗炎活性的类黄酮和花青素。本研究旨在评估开心果对帕金森病(PD)大鼠神经行为和神经化学变化的保护作用。通过注射鱼藤酮(1.5 mg/kg/day,sc)8天诱导PD动物模型。在治疗前和治疗后给予开心果(800 mg/kg/天,口服)两周。在治疗结束时解剖大脑并分离纹状体用于生化和神经化学分析。通过莫里斯水迷宫(MWM)和新物体识别(NOR)测试评估记忆,同时开放场测试(OFT)、孔兹拉倒置屏幕测试(KIST)、杆测试(PT)、光束行走测试(BWT)、斜面测试(IPT)和足迹(FP)测试用于观察运动行为。鱼藤酮给药显着(p  < 0.01) 损害了记忆力,但治疗前和治疗后组的开心果显着改善了记忆力 ( p  < 0.01)。在开心果治疗前后,鱼藤酮引起的运动缺陷显着减弱。补充开心果也显着减弱了由鱼藤酮诱导的氧化应激增加和 DA 和 5-HT 水平降低。此外,在用开心果处理后,注射鱼藤酮的大鼠中升高的载脂蛋白 E (APoE) 水平也正常化。目前的研究结果表明,开心果具有神经保护作用,并通过增加 DA 水平和改善大脑中的氧化状态来改善记忆和运动缺陷。

更新日期:2020-06-11
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