Neuroprotective effects of Alpinia katsumadai against experimental ischemic damage via control of oxidative stress

Pharm Biol. 2013 Feb;51(2):197-205. doi: 10.3109/13880209.2012.716853. Epub 2012 Oct 24.

Abstract

Context: Alpinia katsumadai (Zingiberaceae) has been identified by the National Plant Quarantine Service in Korea. The extract of Alpinia katsumadai seed (EAKS) has antioxidant activities.

Objective: We investigated the neuroprotective effects of EAKS on ischemic damage in the gerbil hippocampal CA1 region after transient cerebral ischemia.

Materials and methods: The ethanol extract of EAKS was obtained by organic solvent, collected in Kangwon province (South Korea) and orally administered using a feeding needle once a day for one week before transient cerebral ischemia in gerbils.

Result: We adapted oral administration of 25 and 50 mg/kg EAKS because there are no data about the absorption and metabolism of EKAS. We found a significant neuroprotection in the 50 mg/kg EAKS-treated ischemia group, not in the 25 mg/kg EAKS-treated ischemia group, at 4 days ischemia-reperfusion (I-R). In the 50 mg/kg EAKS-treated ischemia group, about 68% of pyramidal neurons in the CA1 region were immunostained with neuronal nuclei (NeuN) 4 days after I-R, compared to the vehicle-treated ischemia group. 8-Hydroxy-2'-deoxyguanosine (a marker for DNA damage) and 4-hydroxy-2-nonenal (a marker for lipid peroxidation) immunoreactivity in the CA1 region of the EAKS-treated ischemia group were not markedly changed compared to the vehicle-treated ischemia group. In addition, Cu,Zn- and Mn-SOD immunoreactivity in the CA1 region of the EAKS-treated ischemia group were increased compared to the vehicle-treated ischemia group.

Discussion: Repeated supplements of EAKS could protect neurons against ischemic damage, showing that DNA damage and lipid peroxidation are attenuated and SODs are increased in the ischemic CA1 region.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Administration, Oral
  • Aldehydes / metabolism
  • Alpinia / chemistry*
  • Animals
  • Antioxidants / administration & dosage
  • Antioxidants / isolation & purification
  • Antioxidants / pharmacology*
  • Brain Ischemia / complications
  • Brain Ischemia / drug therapy*
  • Brain Ischemia / metabolism
  • Brain Ischemia / pathology
  • CA1 Region, Hippocampal / blood supply
  • CA1 Region, Hippocampal / drug effects*
  • CA1 Region, Hippocampal / metabolism
  • CA1 Region, Hippocampal / pathology
  • Cytoprotection
  • DNA Damage
  • Disease Models, Animal
  • Ethanol / chemistry
  • Gerbillinae
  • Immunohistochemistry
  • Lipid Peroxidation / drug effects
  • Male
  • Neuroprotective Agents / administration & dosage
  • Neuroprotective Agents / isolation & purification
  • Neuroprotective Agents / pharmacology*
  • Oxidative Stress / drug effects*
  • Plant Extracts / administration & dosage
  • Plant Extracts / isolation & purification
  • Plant Extracts / pharmacology*
  • Plants, Medicinal
  • Reperfusion Injury / etiology
  • Reperfusion Injury / metabolism
  • Reperfusion Injury / pathology
  • Reperfusion Injury / prevention & control*
  • Seeds
  • Solvents / chemistry
  • Superoxide Dismutase / metabolism
  • Time Factors

Substances

  • Aldehydes
  • Antioxidants
  • Neuroprotective Agents
  • Plant Extracts
  • Solvents
  • Ethanol
  • Superoxide Dismutase
  • 4-hydroxy-2-nonenal