Mousavi S Mojtaba, Niazmand Saeed, Hosseini Mahmoud, Hassanzadeh Zarha, Sadeghnia Hamid Reza, Vafaee Farzaneh, Keshavarzi Zakieh
Neurogenic Inflammation Research Center, School of Medicine, Mashhad University of Medical Sciences, Mashhad 9177948564, Iran.
Neurocognitive Research Center, School of Medicine, Mashhad University of Medical Sciences, Mashhad 9177948564, Iran.
Int J Alzheimers Dis. 2015;2015:493729. doi: 10.1155/2015/493729. Epub 2015 Feb 24.
Objective. The effects of hydroalcoholic extract of Teucrium polium and metformin on diabetes-induced memory impairment and brain tissues oxidative damage were investigated. Methods. The rats were divided into: (1) Control, (2) Diabetic, (3) Diabetic-Extract 100 (Dia-Ext 100), (4) Diabetic-Extract 200 (Dia-Ext 200), (5) Diabetic-Extract 400 (Dia-Ext 400), and (6) Diabetic-Metformin (Dia-Met). Groups 3-6 were treated by 100, 200, and 400 mg/kg of the extract or metformin, respectively, for 6 weeks (orally). Results. In passive avoidance test, the latency to enter the dark compartment in Diabetic group was lower than that of Control group (P < 0.01). In Dia-Ext 100, Dia-Ext 200, and Dia-Ext 400 and Metformin groups, the latencies were higher than those of Diabetic group (P < 0.01). Lipid peroxides levels (reported as malondialdehyde, MDA, concentration) in the brain of Diabetic group were higher than Control (P < 0.001). Treatment by all doses of the extract and metformin decreased the MDA concentration (P < 0.01). Conclusions. The results of present study showed that metformin and the hydroalcoholic extract of Teucrium polium prevent diabetes-induced memory deficits in rats. Protection against brain tissues oxidative damage might have a role in the beneficial effects of the extract and metformin.
目的。研究香科科水醇提取物和二甲双胍对糖尿病诱导的记忆障碍及脑组织氧化损伤的影响。方法。将大鼠分为:(1)对照组,(2)糖尿病组,(3)糖尿病-提取物100组(Dia-Ext 100),(4)糖尿病-提取物200组(Dia-Ext 200),(5)糖尿病-提取物400组(Dia-Ext 400),以及(6)糖尿病-二甲双胍组(Dia-Met)。第3 - 6组分别给予100、200和400mg/kg的提取物或二甲双胍,持续6周(口服)。结果。在被动回避试验中,糖尿病组进入暗室的潜伏期低于对照组(P < 0.01)。在Dia-Ext 100、Dia-Ext 200、Dia-Ext 400和二甲双胍组中,潜伏期高于糖尿病组(P < 0.01)。糖尿病组大脑中的脂质过氧化物水平(以丙二醛,MDA,浓度表示)高于对照组(P < 0.001)。所有剂量的提取物和二甲双胍治疗均降低了MDA浓度(P < 0.01)。结论。本研究结果表明,二甲双胍和香科科水醇提取物可预防大鼠糖尿病诱导的记忆缺陷。对脑组织氧化损伤的保护作用可能在提取物和二甲双胍的有益作用中发挥作用。