Inhibitory effects of Dendrobium alkaloids on memory impairment induced by lipopolysaccharide in rats

Planta Med. 2011 Jan;77(2):117-21. doi: 10.1055/s-0030-1250235. Epub 2010 Aug 17.

Abstract

Dendrobium alkaloids (DNLA), extracted from Dendrobium nobile Lindl. whose botanical name is Dendrobium moniliforme, Orchidaceae family, were studied for their effect on lipopolysaccharide (LPS)-induced memory impairment in rats. SD rats were pretreated with DNLA (40, 80, 160 mg/kg/d for 7 d), followed by LPS (50 µg) injection into the right lateral ventricle to produce memory impairment. DNLA treatment continued for another 13 days. The spatial behavior was tested by the Morris water maze; the level of tumor necrosis factor receptor 1 (TNFR1) mRNA was detected by real time RT-PCR, and the protein level of TNFR1, nuclear factor kappa-B (NF- κB) and phosphorylated p38 mitogen-activated protein kinases (p-p38 MAPK) by Western blotting. The results showed that DNLA significantly improved the neurobehavioral performance and prevented LPS-induced elevation in TNFR1 mRNA and protein levels. LPS-induced activation of p38 MAPK and NF- κB pathway was also suppressed. In conclusion, DNLA is effective in protecting against LPS-induced brain impairment, and this effect is due, at least in part, to prevent overexpression of TNFR1 via inhibition of p-p38 MAPK and the downstream NF- κB signal pathway.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alkaloids / pharmacology
  • Alkaloids / therapeutic use*
  • Animals
  • Dendrobium / chemistry*
  • Gene Expression Regulation
  • Hippocampus / drug effects
  • Hippocampus / metabolism
  • Lipopolysaccharides / toxicity*
  • Male
  • Memory Disorders / chemically induced
  • Memory Disorders / drug therapy
  • Memory Disorders / prevention & control*
  • NF-kappa B / biosynthesis
  • NF-kappa B / drug effects
  • Plants, Medicinal / chemistry
  • Rats
  • Rats, Sprague-Dawley
  • Receptors, Tumor Necrosis Factor, Type I / biosynthesis
  • Receptors, Tumor Necrosis Factor, Type I / drug effects
  • Receptors, Tumor Necrosis Factor, Type I / genetics
  • Signal Transduction / drug effects
  • Time Factors
  • p38 Mitogen-Activated Protein Kinases / biosynthesis
  • p38 Mitogen-Activated Protein Kinases / drug effects

Substances

  • Alkaloids
  • Lipopolysaccharides
  • NF-kappa B
  • Receptors, Tumor Necrosis Factor, Type I
  • p38 Mitogen-Activated Protein Kinases