Methanol Extract of Paeonia Japonica Root Protects Cultured Rat Cortical Neurons Against Oxidative Damage Induced by Hydrogen Peroxide

  • Park, Min-Su (College of Veterinary Medicine and Research Institute of herbal Medicine, Chungbuk National University) ;
  • Ban, Ju-Yeon (College of Veterinary Medicine and Research Institute of herbal Medicine, Chungbuk National University) ;
  • Lee, Ju-Hyun (College of Veterinary Medicine and Research Institute of herbal Medicine, Chungbuk National University) ;
  • Song, Kyung-Sik (College of Agriculture and Life-Sciences, Kyungpook National University) ;
  • Seong, Yeon-Hee (College of Veterinary Medicine and Research Institute of herbal Medicine, Chungbuk National University)
  • Published : 2006.04.01

Abstract

Paeoniae radix has been widely used for its anti-allergic, anti-inflammatory and analgesic effects, and demonstrated to have anticonvulsant, memory enhancing and anxiolytic activities. The present study was performed to examine the protective effect of methanol extract of Paeoniae radix (PR) from Paeoniae Japonica Miyabe et Takeda (Paeoniaceae) on hydrogen peroxide $(H_2O_2)-induced$ neurotoxicity using cultured rat cerebral cortical neuron. $H_2O_2$ produced a concentration-dependent reduction of neuronal viability, PR, over a concentration range of 10 to $100\;{\mu}g/ml$ showed concentration-dependent decrease of the $H_2O_2$$(100\;{\mu}M)-induced$ neuronal cell death, as assessed by a 3-[4,5-dimethylthiazol-2-yl]-2,5-di-phenyl-tetrazolium bromide assay and the number of apoptotic nuclei, evidenced by Hoechst 33342 staining. PR $(100\;{\mu}g/ml$ inhibited $100\;{\mu}M$ $H_2O_2-induced$ elevation of the cytosolic $Ca^{2+}$ concentration $([Ca^{2+}]_c)$, which was measured by a fluorescent dye, flue-4 AM. PR $(50\;{\mu}g/ml$ inhibited glutamate release into medium induced by $100\;{\mu}M$ $H_2O_2$, which was measured by HPLC, and generation of reactive oxygen species (ROS). These results suggest that PR may mitigate the $H_2O_2-induced$ neurotoxiciy by interfering with the increase of $[Ca^{2+}]_c$, and then inhibiting glutamate release and generation of ROS in cultured neurons.

Keywords

References

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