Actinidia arguta Protects Cultured Cerebral Cortical Neurons against Glutamate-Induced Neurotoxicity via Inhibition of $[Ca^{2+}]_i$ Increase and ROS Generation

  • Cho, Jae-Hee (College of Veterinary Medicine, Chungbuk National University) ;
  • Lee, Hong-Kyu (College of Veterinary Medicine, Chungbuk National University) ;
  • Seong, Yeon-Hee (College of Veterinary Medicine, Chungbuk National University)
  • Received : 2011.12.19
  • Accepted : 2012.02.24
  • Published : 2012.03.31

Abstract

Actinidia arguta (Actinidiaceae) has been reported to have several pharmacological effects such as anti-inflammatory, anti-allergic, and anti-oxidant activities. The present study investigated the protective activity of an ethanol extract from the leaf and stem of A. arguta against glutamate-induced neurotoxicity using cultured rat cortical neurons. Exposure of cultured cortical neurons to $500{\mu}M$ glutamate for 12 h triggered neuronal cell death. A. arguta inhibited glutamate-induced neuronal death and apoptosis, which were measured by a 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl-tetrazolium bromide (MTT) assay and Hoechst 33342 staining, respectively. The increase of pro-apoptotic proteins, Bax and c-caspase-3, in glutamate-treated neurons was significantly inhibited by treatment with A. arguta. A. arguta also inhibited $500{\mu}M$ glutamate-induced elevation of intracellular calcium concentration ($[Ca^{2+}]_i$) and reactive oxygen species (ROS) generation, which were measured by fluorescent dyes, Fluo-4 AM and $H_2DCF$-DA, respectively. These results suggest that A. arguta may prevent glutamate-induced apoptotic neuronal death by inhibiting $[Ca^{2+}]_i$ elevation and ROS generation and, therefore, may have a therapeutic role for the prevention of neurodegeneration in cerebral ischemic diseases.

Keywords

References

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