Bee Venom Suppresses Ischemia-induced Increment of Apoptosis and Cell Proliferation in Hippocampal Dentate Gyrus

  • Lim Baek Vin (Department of Oriental Pharmaceutical Science, College of Pharmacy, Kyunghee University) ;
  • Lee Choong Yeol (Department of Physiology, College of Oriental Medicine, Kyungwon University) ;
  • Kang Jin Oh (Department of Radiation Oncology, College of Medicine, Kyunghee University) ;
  • Kim Chang Ju (Department of Physiology, College of Medicine, Kyunghee University) ;
  • Cho Sonhae (Department of Oriental Pharmaceutical Science, College of Pharmacy, Kyunghee University)
  • 발행 : 2004.02.01

초록

Cerebral ischemia resulting from transient or permanent occlusion of cerebral arteries leads to neuronal cell death and eventually causes neurological impairments. Bee venom has been used for the treatment inflammatory disease. In the present study, the effects of bee venom on apoptosis and cell proliferation in the hippocampal dentate gyrus following transient global ischemia in gerbils were investigated using immunohistochemistry for cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2), caspase-3, and 5-bromo-2'-deoxyuridine (BrdU). It was shown that apoptotic cell death and cell proliferation in the hippocampal dentate gyrus were significantly increased following transient global ischemia in gerbils and that treatment of bee venom suppressed the ischemia-induced increase in apoptosis and cell proliferation in the dentate gyrus. The present results also showed that 1 mg/kg bee-venom treatment suppressed the ischemia-induced increasing apoptosis, cell proliferation, and COX-2 expression in the dentate gyrus. It is possible that the suppression of cell proliferation is due to the reduction of apoptotic cell death by treatment of bee venom. In the present study, bee venom was shown to prosses anti-apoptotic effect in ischemic brain disease, and this protective effect of bee venom against ischemia-induced neuronal cell death is closely associated with suppression on caspase-3 expression.

키워드

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