BACKGROUND: In this study, the neuroprotective effects of caffeic acid phenethyl ester (CAPE) in the hippocampus of cigarette smoke exposed rabbits were investigated. MATERIALS AND METHODS: Eighteen rabbits were used as experimental subjects and divided into three equal groups. The control group (Group A) was exposed to clean air. Rabbits in the cigarette smoke (CS) group (Group B) were exposed to cigarette smoke 1 hour daily in a room within a glass chamber for 4 weeks. Animals in the CS+CAPE group (Group C) were exposed to cigarette smoke as in Group B and administered CAPE (10 micromol/kg/day) intraperitoneally for 4 weeks just before the exposure to cigarette smoke. Rabbits in all three groups were sacrificed with intraperitoneal administration of 100 mg/kg sodium pentothal and their brains were removed immediately. In the hippocampal formation samples of left hemispheres, the levels of malondialdehyde (MDA) and superoxide dismutase (SOD) were measured and the number of apoptotic neurons was counted by 'terminal transferase dUTP nick end labelling' (TUNEL) assay in the right hippocampal formation. RESULTS: We found that MDA levels increased significantly in the Group B rabbits compared with the control group (Group A; p = 0.001). In contrast, SOD activities decreased significantly in Group B rabbits compared with the control group (p = 0.001). In the CAPE treated rabbits (Group C), MDA levels decreased and SOD activities increased significantly as compared with Group B rabbits (p = 0.002, p = 0.002, respectively). The number of apoptotic neurons (TUNEL+) in the CA1, CA2, CA3 and dentate gyrus areas of rabbits' hippocampal formation were significantly increased in Group B rabbits compared with the control group. On the other hand, the number of apoptotic neurons in the hippocampus areas was decreased significantly in Group C rabbits compared with Group B rabbits. CONCLUSION: These findings suggest that cigarette smoking induces apoptosis in the hippocampal formation of rabbits and CAPE has a protective role against this induction.
BACKGROUND: In this study, the neuroprotective effects of caffeic acid phenethyl ester (CAPE) in the hippocampus of cigarette smoke exposed rabbits were investigated. MATERIALS AND METHODS: Eighteen rabbits were used as experimental subjects and divided into three equal groups. The control group (Group A) was exposed to clean air. Rabbits in the cigarette smoke (CS) group (Group B) were exposed to cigarette smoke 1 hour daily in a room within a glass chamber for 4 weeks. Animals in the CS+CAPE group (Group C) were exposed to cigarette smoke as in Group B and administered CAPE (10 micromol/kg/day) intraperitoneally for 4 weeks just before the exposure to cigarette smoke. Rabbits in all three groups were sacrificed with intraperitoneal administration of 100 mg/kg sodium pentothal and their brains were removed immediately. In the hippocampal formation samples of left hemispheres, the levels of malondialdehyde (MDA) and superoxide dismutase (SOD) were measured and the number of apoptotic neurons was counted by 'terminal transferase dUTP nick end labelling' (TUNEL) assay in the right hippocampal formation. RESULTS: We found that MDA levels increased significantly in the Group B rabbits compared with the control group (Group A; p = 0.001). In contrast, SOD activities decreased significantly in Group B rabbits compared with the control group (p = 0.001). In the CAPE treated rabbits (Group C), MDA levels decreased and SOD activities increased significantly as compared with Group B rabbits (p = 0.002, p = 0.002, respectively). The number of apoptotic neurons (TUNEL+) in the CA1, CA2, CA3 and dentate gyrus areas of rabbits' hippocampal formation were significantly increased in Group B rabbits compared with the control group. On the other hand, the number of apoptotic neurons in the hippocampus areas was decreased significantly in Group C rabbits compared with Group B rabbits. CONCLUSION: These findings suggest that cigarette smoking induces apoptosis in the hippocampal formation of rabbits and CAPE has a protective role against this induction.