Effect of EA on Cerebral Ischemia-reperfusion Induced Changes of P53 Protein Expression in Cerebral Cortex of Elder Rats
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Effect of EA on Cerebral Ischemia-reperfusion Induced Changes of P53 Protein Expression in Cerebral Cortex of Elder Rats
Acupuncture ResearchIssue 4, Pages: 255-257(2003)
作者机构:
江苏省徐州医学院附属医院神经内科
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Published:2003
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Effect of EA on Cerebral Ischemia-reperfusion Induced Changes of P53 Protein Expression in Cerebral Cortex of Elder Rats[J]. Acupuncture research, 2003, (4): 255-257.
DOI:
Effect of EA on Cerebral Ischemia-reperfusion Induced Changes of P53 Protein Expression in Cerebral Cortex of Elder Rats[J]. Acupuncture research, 2003, (4): 255-257.DOI:
Effect of EA on Cerebral Ischemia-reperfusion Induced Changes of P53 Protein Expression in Cerebral Cortex of Elder Rats
这可能是电针抗脑缺血后神经元凋亡的途径之一Objective:To observe the effect of electroacupuncture( EA) on P53 p rotein expression in rats with cerebral ischemia-reperfusion injury and to anal yze the mechanisms of EA in reducing neuronal apoptosis. Method: 36 S D rats were randomly and evenly divided into sham-operation group
model group an d EA group.Cerebral ischemia-reperfusion model was established by using modifie d (Pulsinelli's)4-vessel occlusion method. Bilateral"Zusanli"(ST 36) were pu nctured and stimulated with an EA therapeutic apparatus (100 Hz
3.5 mA and dura tion of 60 min)
once a day
3 days altogether. Immunohistochemical method was use d to display P53 protein expression in the cerebral cortex of elder rats with ce rebral ischemia-reperfusion injury. Results: Compared with sham-ope r ation group
the number of P53 immuno-reaction positive cells markedly increased in ischemia-reperfusion group ( P <0.05). In EA group
the number of P53 imm uno-reaction positive cells was significantly fewer than that of model group ( P <0.0 5)
suggesting that EA could down-regulate P53 protein expression in rats with c erebral ischemia-reperfusion. Conclusion:EA could down-regulate P53 protein expression in cerebral ischemia rats
that may contribute to the actio n of EA in reducing cerebral neuronal apoptosis.