Khan Muhammad Zahid, Atlas Nagina, Nawaz Waqas
Department of Pharmacology, China Pharmaceutical University, Nanjing 210009, China; Department of Biotechnology, University of science and technology Bannu, K.P.K, Pakistan.
Department of Bioinformatics and Biotechnology, Faculty of basic and applied sciences. International Islamic university Islamabad, Pakistan.
Biomed Pharmacother. 2016 Dec;84:387-394. doi: 10.1016/j.biopha.2016.09.055. Epub 2016 Sep 23.
Cognitive deficiency and oxidative stress have been well documented in aging disorders including Alzheimer's disease. The aim of this study was to investigate the therapeutic efficacy of Caralluma tuberculata methanolic extract (CTME) on cognitive impairment in mice induced with d-galactose. In this study we assessed the therapeutic efficacy of CTME on cognitive impairment in mice induced with d-galactose by conduction of behavioral and cognitive performance tests. In order to explore the possible role of CTME against d-galactose-induced oxidative damages, various biochemical indicators were assessed. Chronic administration of d-galactose (150mg/kgd, s.c.) for 7 weeks significantly impaired cognitive performance (in step-through passive, active avoidance test, Hole-Board test, Novel object recognition task and Morris water maze) and oxidative defense as compared to the control group. The results revealed that CTME treatment for two weeks (100, 200 and 300mg/kg p.o) significantly ameliorated cognitive performance and oxidative defense. All groups of CTME enhanced the learning and memory ability in step-through passive, active avoidance test, Hole-Board test Novel object recognition task and Morris water maze. Furthermore, high and middle level of CTME (300 and 200mg/kg p.o) significantly increased Total antioxidative capacity (T-AOC), Glutathione peroxidase (GSH-Px), superoxide dismutase (SOD) activity, neprilysin (NEP), and β-site AβPP cleaving enzyme 1 (BACE1) expression while Nitric Oxide (NO), Nitric Oxide Synthase (NOS) activity and Malondialdehyde (MDA) concentration, and the level of Aβ1-42 and presenilin 1 (PS1) were decreased. The present study showed that CTME have a significant relieving effect on learning, memory and spontaneous activities in d-galactose-induced mice model, and ameliorates cognitive impairment and biochemical dysfunction in mice.
认知缺陷和氧化应激在包括阿尔茨海默病在内的衰老性疾病中已有充分记录。本研究的目的是探讨瘤状肉珊瑚甲醇提取物(CTME)对d - 半乳糖诱导的小鼠认知障碍的治疗效果。在本研究中,我们通过进行行为和认知能力测试,评估了CTME对d - 半乳糖诱导的小鼠认知障碍的治疗效果。为了探究CTME对抗d - 半乳糖诱导的氧化损伤的可能作用,我们评估了各种生化指标。与对照组相比,连续7周皮下注射d - 半乳糖(150mg/kg·d)显著损害了认知能力(在穿梭箱被动、主动回避试验、洞板试验、新物体识别任务和莫里斯水迷宫试验中)以及氧化防御能力。结果显示,CTME连续两周灌胃给药(100、200和300mg/kg)显著改善了认知能力和氧化防御能力。CTME各给药组均提高了穿梭箱被动、主动回避试验以及洞板试验、新物体识别任务和莫里斯水迷宫试验中的学习和记忆能力。此外,CTME高剂量组(300mg/kg灌胃)和中剂量组(200mg/kg灌胃)显著提高了总抗氧化能力(T - AOC)、谷胱甘肽过氧化物酶(GSH - Px)、超氧化物歧化酶(SOD)活性、中性内肽酶(NEP)以及β - 淀粉样前体蛋白裂解酶1(BACE1)的表达,同时降低了一氧化氮(NO)、一氧化氮合酶(NOS)活性和丙二醛(MDA)浓度,以及β - 淀粉样蛋白1 - 42(Aβ1 - 42)和早老素1(PS1)的水平。本研究表明,CTME对d - 半乳糖诱导的小鼠模型的学习、记忆和自发活动具有显著的缓解作用,并改善了小鼠的认知障碍和生化功能障碍。