Dadgar Masoumeh, Pouramir Mahdi, Dastan Zohreh, Ghasemi-Kasman Maryam, Ashrafpour Manouchehr, Moghadamnia Ali Akbar, Khafri Soraya, Pourghasem Mohsen
Student Research Committee, Babol University of Medical Sciences, Babol, Iran.
Department of Clinical Biochemistry, Faculty of Medicine, Babol University of Medical Sciences, Babol, Iran.
Avicenna J Phytomed. 2018 Nov-Dec;8(6):533-542.
Arbutin has been shown to have antioxidant and free-radical scavenging properties. The aim of this study was to investigate the effects of arbutin administration on behavioral impairment, and oxidative and nitrosative stress in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced animal model of Parkinson's disease (PD).
PD model was developed by 4 intraperitoneal (i.p.) injections of MPTP (20 mg/kg) with 2 h intervals in mice. Experimental groups received once daily injection of saline as vehicle (control group) or arbutin (50 mg/kg, i.p.) one week before MPTP injections and this protocol was continued seven days post lesion. Behavioral deficits were evaluated using locomotion test, hanging wire test and forepaw stride length. Parameters indicating the oxidation levels including lipid peroxidation marker (TBARS), nitrite, protein carbonyl levels and antioxidant activity including ferric reducing antioxidant power (FRAP) were assessed in serum and midbrain samples.
Treatment with arbutin improved motor functions in an MPTP-induced PD model compared to control group (p<0.001). Mice treated with MPTP showed reduced levels of FRAP (p<0.001) and increased levels of TBARS (p<0.001), nitrite (p<0.001) and protein carbonyl (p<0.01), compared to the control group. In contrast to the MPTP group, arbutin treatment decreased the levels of TBARS (p<0.05), nitrite (p<0.05), protein carbonyl (p<0.05), and increased FRAP levels (p<0.05) in mice with PD.
These findings suggest that arbutin attenuates the behavioral impairment and oxidative stress in a PD animal model.
已证明熊果苷具有抗氧化和清除自由基的特性。本研究的目的是调查在1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)诱导的帕金森病(PD)动物模型中,给予熊果苷对行为障碍以及氧化应激和亚硝化应激的影响。
通过给小鼠腹腔注射4次MPTP(20mg/kg),间隔2小时,建立PD模型。实验组在MPTP注射前一周每天注射一次生理盐水作为溶媒(对照组)或熊果苷(50mg/kg,腹腔注射),该方案在损伤后持续7天。使用运动测试、悬线测试和前爪步幅长度评估行为缺陷。在血清和中脑样本中评估指示氧化水平的参数,包括脂质过氧化标志物(TBARS)、亚硝酸盐、蛋白质羰基水平,以及指示抗氧化活性的参数,包括铁还原抗氧化能力(FRAP)。
与对照组相比,在MPTP诱导的PD模型中,熊果苷治疗改善了运动功能(p<0.001)。与对照组相比,用MPTP治疗的小鼠FRAP水平降低(p<0.001),TBARS(p<0.001)、亚硝酸盐(p<0.001)和蛋白质羰基(p<0.01)水平升高。与MPTP组相反,熊果苷治疗降低了PD小鼠的TBARS(p<0.05)、亚硝酸盐(p<0.05)、蛋白质羰基(p<0.05)水平,并提高了FRAP水平(p<0.05)。
这些发现表明,熊果苷可减轻PD动物模型中的行为障碍和氧化应激。