OBJECTIVE: To observe the expression of amyloid beta precursor protein and amyloid beta protein in neurons of hippocampal CA1 region after brain ischemia in human. METHODS: Neuronal damage was examined by using HE staining, and expression of APP and Abeta(1-40) was determined by immunohistochemistry in the hippocampal CA1 region of the brain specimens of 43 patients who died 2 h-6 h, 7 h-24 h, 25 h-48 h, 49 h-72 h, 73 h-96 h, 97 h-144 h, or 145 h-168 h after cerebral ischemia and in 2 specimens of patients who died of other diseases as control group. RESULTS: The expression of Abeta(1-40) was 25.07 +/- 2.79 in the specimens 2 h-6 h after cerebral ischemia, peaked 73 h-96 h after cerebral ischemia (33.22 +/- 2.67), then decreased till 145 h-168 h after cerebral ischemia, however, all higher than that in the control group (2.88 +/- 0.18, all P < 0.05). The expression of beta-APP was 33.30 +/- 0.42 2 h-6 h after cerebral ischemia, was 28.11 +/- 2.03 7 h-24 h after cerebral ischemia, increased to peak value (32.32 +/- 1.36) 73 h-96 h after cerebral ischemia, and then decreased to 28.48 +/- 2.01, all higher than that of the control group (25.90 +/- 1.55) with significant differences between those 2 h-6 h and 73 h-96 h after ischemia and that of the control group (both P < 0.01). The increase of beta-APP was positively correlated with the expression of Abeta(1-40) 24 h after ischemia. CONCLUSION: The expression of beta-APP and that of Abeta(1-40) are up-regulated after cerebral ischemia, thus aggravating cerebral ischemia.
OBJECTIVE: To observe the expression of amyloid beta precursor protein and amyloid beta protein in neurons of hippocampal CA1 region after brain ischemia in human. METHODS: Neuronal damage was examined by using HE staining, and expression of APP and Abeta(1-40) was determined by immunohistochemistry in the hippocampal CA1 region of the brain specimens of 43 patients who died 2 h-6 h, 7 h-24 h, 25 h-48 h, 49 h-72 h, 73 h-96 h, 97 h-144 h, or 145 h-168 h after cerebral ischemia and in 2 specimens of patients who died of other diseases as control group. RESULTS: The expression of Abeta(1-40) was 25.07 +/- 2.79 in the specimens 2 h-6 h after cerebral ischemia, peaked 73 h-96 h after cerebral ischemia (33.22 +/- 2.67), then decreased till 145 h-168 h after cerebral ischemia, however, all higher than that in the control group (2.88 +/- 0.18, all P < 0.05). The expression of beta-APP was 33.30 +/- 0.42 2 h-6 h after cerebral ischemia, was 28.11 +/- 2.03 7 h-24 h after cerebral ischemia, increased to peak value (32.32 +/- 1.36) 73 h-96 h after cerebral ischemia, and then decreased to 28.48 +/- 2.01, all higher than that of the control group (25.90 +/- 1.55) with significant differences between those 2 h-6 h and 73 h-96 h after ischemia and that of the control group (both P < 0.01). The increase of beta-APP was positively correlated with the expression of Abeta(1-40) 24 h after ischemia. CONCLUSION: The expression of beta-APP and that of Abeta(1-40) are up-regulated after cerebral ischemia, thus aggravating cerebral ischemia.