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Published:2007
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[1].ISCHEMIC PRECONDITIONING RELIEVES ISCHEMIA/REPERFUSION INJURY OF HIPPOCAMPUS NEURONS IN RAT BY INHIBITING p53 AND BAX EXPRESSIONS[J].Chinese Medical Sciences Journal,2007(02):123-127.
Hui-min Liu1, 2, Jing-xin Li1, et al. ISCHEMIC PRECONDITIONING RELIEVES ISCHEMIA/REPERFUSION INJURY OF HIPPOCAMPUS NEURONS IN RAT BY INHIBITING p53 AND BAX EXPRESSIONS[J]. Chinese medical sciences journal, 2007, (2): 123-127.
[1].ISCHEMIC PRECONDITIONING RELIEVES ISCHEMIA/REPERFUSION INJURY OF HIPPOCAMPUS NEURONS IN RAT BY INHIBITING p53 AND BAX EXPRESSIONS[J].Chinese Medical Sciences Journal,2007(02):123-127. DOI:
Hui-min Liu1, 2, Jing-xin Li1, et al. ISCHEMIC PRECONDITIONING RELIEVES ISCHEMIA/REPERFUSION INJURY OF HIPPOCAMPUS NEURONS IN RAT BY INHIBITING p53 AND BAX EXPRESSIONS[J]. Chinese medical sciences journal, 2007, (2): 123-127. DOI:
Objective To examine whether ischemic preconditioning (IPC) can protect neuron against delayed death in CA1 subfield of hippocampus following reperfusion of a lethal ischemia in rats
and explore the role of p53 and bax in this process. Methods We examined the effect of IPC on delayed neuron death
neuron apoptosis
expressions of p53 and bax gene in the CA1 area of hippocampus in the rats using HE staining
flow cytometry
RT-PCR
and immunohistochemistry technique. Results IPC enhanced the quantity of survival cells in the CA1 region of hippocampus (216±9 cells/0.72 mm2 vs. 30±5 cells/0.72 mm2
P<0.01)
decreased the percentages of apoptotic neurons of hippocampus caused by ischemia/reperfusion (2.06%±0.21% vs. 4.27%±0.08%
P<0.01)
and weakened the expressions of p53 and bax gene of hippocampus compared with ischemia/reperfusion without IPC. Conclusion IPC can protect the neurons in the CA1 region of hippocampus against apoptosis caused by ische- mia/reperfusion
and this process may be related to the reduced expressions of p53 and bax.
Objective To examine whether ischemic preconditioning (IPC) can protect neuron against delayed death in CA1 subfield of hippocampus following reperfusion of a lethal ischemia in rats
and explore the role of p53 and bax in this process. Methods We examined the effect of IPC on delayed neuron death
neuron apoptosis
expressions of p53 and bax gene in the CA1 area of hippocampus in the rats using HE staining
flow cytometry
RT-PCR
and immunohistochemistry technique. Results IPC enhanced the quantity of survival cells in the CA1 region of hippocampus (216±9 cells/0.72 mm2 vs. 30±5 cells/0.72 mm2
P<0.01)
decreased the percentages of apoptotic neurons of hippocampus caused by ischemia/reperfusion (2.06%±0.21% vs. 4.27%±0.08%
P<0.01)
and weakened the expressions of p53 and bax gene of hippocampus compared with ischemia/reperfusion without IPC. Conclusion IPC can protect the neurons in the CA1 region of hippocampus against apoptosis caused by ische- mia/reperfusion
and this process may be related to the reduced expressions of p53 and bax.
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