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      Gingko biloba extract (EGb 761) prevents increase of Bad-Bcl-XL interaction following cerebral ischemia.

      The American journal of Chinese medicine
      Animals, Apoptosis, drug effects, Blotting, Western, Brain Ischemia, metabolism, prevention & control, Cerebral Cortex, blood supply, Ginkgo biloba, chemistry, Immunoprecipitation, In Situ Nick-End Labeling, Male, Neuroprotective Agents, pharmacology, Phytotherapy, Plant Extracts, Poly(ADP-ribose) Polymerases, Protein Binding, Rats, Rats, Sprague-Dawley, bcl-Associated Death Protein, bcl-X Protein

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          Abstract

          A standardized extract of Gingko biloba, EGb 761, has been shown to exert a neuroprotective effect against permanent and transient focal cerebral ischemia. This study investigated whether EGb 761 modulates Bcl-2 family proteins in ischemic brain injury. Male adult rats were treated with EGb 761 (100 mg/kg) or vehicle prior to middle cerebral artery occlusion (MCAO), brain tissues were collected 24 hours after MCAO. EGb761 administration significantly decreased the number of TUNEL-positive cells in the cerebral cortex. Ischemic brain injury induced decrease of Bcl-2 and Bcl-X(L) levels. EGb 761 prevented not only the injury-induced decrease of Bcl-2 and Bcl-X(L) levels, but also the injury-induced increase of Bax. Moreover, in the presence of EGb 761, the interaction of Bad and Bcl-X(L) decreased compared to that of vehicle-treated animals. In addition, EGb 761 prevented the injury-induced increase of cleaved PARP. The finding suggests that EGb 761 prevents cell death against ischemic brain injury and EGb 761 neuroprotection is affected by preventing the injury-induced increase of Bad and Bcl-X(L) interaction.

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