Planta Med 2010; 76(1): 20-26
DOI: 10.1055/s-0029-1185903
Pharmacology
Original Papers
© Georg Thieme Verlag KG Stuttgart · New York

Neuroprotective Effect of Defatted Sesame Seeds Extract against in vitro and in vivo Ischemic Neuronal Damage

Nirmala Jamarkattel-Pandit1 , Naba Raj Pandit1 , Mi-Yeon Kim1 , 2 , Si Hyung Park3 , Kwan Su Kim3 , Hoyoung Choi1 , Hocheol Kim1 , 2 , Youngmin Bu1
  • 1Department of Herbal Pharmacology, College of Oriental Medicine, Kyung Hee University, Seoul, Korea
  • 2Korea Institute of Science and Technology for Eastern Medicine (KISTEM), Neumed Co., Ltd., Seoul, Korea
  • 3Division of Bioscience, College of Natural Science, Mokpo National University, Muan, Korea
Weitere Informationen

Publikationsverlauf

received Dec. 18, 2008 revised June 5, 2009

accepted June 10, 2009

Publikationsdatum:
13. Juli 2009 (online)

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Abstract

Sesame (Sesamum indicum L.) is an important oilseed crop that possesses a wide spectrum of pharmacological activities. Many studies have been conducted to investigate its health-promoting effects. Compared to other plant oils, sesame seed oil is highly stable to oxidation and has been demonstrated to have protective effects against ischemia-reperfusion injury in the rat brain. However; the effects of defatted sesame seeds extract (DSE) have not been studied yet. The purpose of this study was to evaluate the protective effect of DSE against ischemia models. For in vitro ischemia, oxygen-glucose deprivation followed by reoxygenation (OGD‐R, 4 h OGD followed by 24 h reoxygenation) in HT22 cells was used to investigate the protective effects on cell death and the inhibitory effects on lipid peroxidation. For in vivo ischemia, the middle cerebral artery occlusion (MCAo, 2 h of MCAo followed by 22 h of reperfusion) rat model was used. Twenty-two h after occlusion the rats were assessed for neurobehavioral deficit and infarct volume. DSE (0.1–10 µg/mL) significantly reduced the cell death and inhibited lipid peroxidation induced by OGD‐R. DSE (30, 100 and 300 mg/kg, p. o.) given twice at 0 h and 2 h after onset of ischemia reduced brain infarct volume dose-dependently and improved sensory-motor function. The therapeutic time window of DSE (300 mg/kg, p. o.) was 2 h after MCAo in rats. In conclusion, our results show that DSE may be effective in ischemia models by an antioxidative mechanism.

References

Prof. Youngmin Bu

Department of Herbal Pharmacology
College of Oriental Medicine
Kyung Hee University

Seoul 130-701

Korea

Telefon: + 82 29 61 94 62

Fax: + 82 29 64 03 25

eMail: ymbu@khu.ac.kr