神经病学和神经科学杂志

  • 国际标准期刊号: 2171-6625
  • 期刊 h 指数: 17
  • 期刊引用分数: 4.43
  • 期刊影响因子: 3.38
索引于
  • 打开 J 门
  • Genamics 期刊搜索
  • 全球影响因子 (GIF)
  • 中国知网(CNKI)
  • 研究期刊索引目录 (DRJI)
  • OCLC-WorldCat
  • 普罗奎斯特传票
  • 科学期刊影响因子 (SJIF)
  • 欧洲酒吧
  • 谷歌学术
  • 秘密搜索引擎实验室
分享此页面

抽象的

Lupeol Isolated from Betula alnoides Ameliorates Amyloid Beta Induced Neuronal Damage via Targeting Various Pathological Events and Alteration in Neurotransmitter Levels in Rat’s Brain

Madhu Kaundal, Mohd Akhtar and Rahul Deshmukh

Lupeol, a natural active constituent of Betula alnoides (BA), is well known for its anti-inflammatory, anti-oxidant and neuroprotective activities. In present study the therapeutic potential of lupeol was investigated against amyloid beta (Aβ (1-42)) induced cognitive deficit, neurochemical and biochemical abnormalities in rats. Lupeol was isolated from the BA and its structure was confirmed through nuclear magnetic resonance spectra. Aβ (1-42) (4 μg/4 μL) intracerebroventrically (icv) was administered to rats for the induction of Alzheimer's disease (AD). Lupeol treatment (25 mg/kg/day, 50 mg/kg/day and 100 mg/kg/day per orally) was started one week after Aβ (1-42) infusion up to the 21st days. Morris water maze from day 16 to 21 and object recognition tasks on day 14 and 15 were performed for memory assessment. On 22nd day, animals were sacrificed and hippocampi were isolated for analysis of biochemical (acetylcholinesterase, lipid hydroperoxide, glutathione and nitrite) and neuro-inflammatory (tumor necrosis factor -α, interleukin (IL)-1β, and IL-6) parameters. In the present study Aβ (1-42) infusion was significantly impaired behavioral memory, increased oxidative stress, decreased antioxidant enzyme and increased pro-inflammatory markers. Treatment of lupeol significantly restored Aβ (1-42) induced behavioral and biochemical abnormalities in rats brain. The findings of the present study suggest that lupeol act through multiple mechanisms and would be used to curb cognitive decline associated with neurodegenerative disorders of AD.