Department of Veterinary Physiology and Biochemistry, University of Ibadan, Ibadan, Nigeria.
Department of Veterinary Anatomy, University of Ibadan, Ibadan, Nigeria.
Brain Behav. 2018 Jul;8(7):e01014. doi: 10.1002/brb3.1014. Epub 2018 Jun 1.
Exposures to toxic levels of vanadium and soluble vanadium compounds cause behavioral impairments and neurodegeneration via free radical production. Consequently, natural antioxidant sources have been explored for effective and cheap remedy following toxicity. Grewia carpinifolia has been shown to improve behavioral impairments in vanadium-induced neurotoxicity, however, the active compounds implicated remains unknown. Therefore, this study was conducted to investigate ameliorative effects of bioactive compounds from G. carpinifolia on memory and behavioral impairments in vanadium-induced neurotoxicity.
Sixty BALB/c mice were equally divided into five groups (A-E). A (control); administered distilled water, B (standard); administered α-tocopherol (500 mg/kg) every 72 hr orally with daily dose of sodium metavanadate (3 mg/kg) intraperitoneally, test groups C, and D; received single oral dose of 100 μg β-spinasterol or stigmasterol (bioactive compounds from G. carpinifolia), respectively, along with sodium metavanadate and the model group E, received sodium metavanadate only for seven consecutive days. Memory, locomotion and muscular strength were accessed using Morris water maze, Open field and hanging wire tests. In vivo antioxidant and neuroprotective activities were evaluated by measuring catalase, superoxide dismutase, MDA, H O , and myelin basic protein (MBP) expression in the hippocampus.
In Morris water maze, stigmasterol significantly (p ≤ 0.05) decreased escape latency and increased swimming time in target quadrant (28.01 ± 0.02; 98.24 ± 17.38 s), respectively, better than α-tocopherol (52.43 ± 13.25; 80.32 ± 15.21) and β-spinasterol (42.09 ± 14.27; 70.91 ± 19.24) in sodium metavanadate-induced memory loss (112.31 ± 9.35; 42.35 ± 11.05). β-Spinasterol and stigmasterol significantly increased exploration and latency in open field and hanging wire tests respectively. Stigmasterol also increased activities of antioxidant enzymes, decreased oxidative stress markers and lipid peroxidation in mice hippocampal homogenates, and increased MBP expression.
The findings of this study indicate a potential for stigmasterol, a bioactive compound from G. carpinifolia in improving cognitive decline, motor coordination, and ameliorating oxidative stress in vanadium-induced neurotoxicity.
接触到有毒水平的钒和可溶性钒化合物会通过自由基的产生导致行为损伤和神经退行性变。因此，人们一直在探索天然抗氧化剂来源，以寻找有效的廉价补救方法。研究表明，山芝麻可改善钒诱导的神经毒性中的行为损伤，但涉及的活性化合物仍不清楚。因此，本研究旨在探讨山芝麻中的生物活性化合物对钒诱导的神经毒性中的记忆和行为损伤的改善作用。
将 60 只 BALB/c 小鼠等分为五组（A-E）。A（对照组）；给予蒸馏水，B（标准组）；给予α-生育酚（500mg/kg），每 72 小时口服一次，同时每天腹膜内注射偏钒酸钠（3mg/kg），测试组 C 和 D；分别给予 100μgβ-菠菜甾醇或豆甾醇（山芝麻中的生物活性化合物）单一口服剂量，与偏钒酸钠一起，模型组 E 仅连续 7 天给予偏钒酸钠。使用 Morris 水迷宫、旷场和悬线试验评估记忆、运动和肌肉力量。通过测量海马中的过氧化氢酶、超氧化物歧化酶、丙二醛、H 2 O 2 和髓鞘碱性蛋白（MBP）的表达，评估体内抗氧化和神经保护活性。
在 Morris 水迷宫中，豆甾醇显著（p≤0.05）降低逃避潜伏期并增加目标象限的游泳时间（28.01±0.02；98.24±17.38 s），优于α-生育酚（52.43±13.25；80.32±15.21）和β-菠菜甾醇（42.09±14.27；70.91±19.24）在偏钒酸钠诱导的记忆丧失中（112.31±9.35；42.35±11.05）。β-菠菜甾醇和豆甾醇分别显著增加了旷场和悬线试验中的探索和潜伏期。豆甾醇还增加了抗氧化酶的活性，降低了小鼠海马匀浆中的氧化应激标志物和脂质过氧化产物，增加了 MBP 的表达。
本研究结果表明，山芝麻中的生物活性化合物豆甾醇具有改善认知能力下降、运动协调能力和改善钒诱导的神经毒性中的氧化应激的潜力。
