学术
大鼠局灶性脑缺血再灌注中nNOS源性NO对Bcl-2、Bax表达的影响
李莉[1] 尹青[1] 罗波[2] 李陈莉[1] 王慧娟[1] 马洪骏[1]
[1]河北医科大学组织胚胎学教研室,石家庄050017 [2]石家庄裕华西路卫生院,石家庄050017
摘 要:
为研究大鼠局灶性脑缺血再灌注早期神经元型一氧化氮合酶（nNOS）来源的一氧化氮（NO）和过氧亚硝基阴离子（ONOO^-）对Bcl-2和Bax蛋白表达的影响，本实验闭塞大鼠左侧大脑中动脉造成局灶性脑缺血模型，给予选择性nNOS抑制剂。7硝基吲唑，应用免疫组化法检测Bcl-2和Bax蛋白表达的变化。结果表明：50mg／kg．25mg／kg剂量的7-硝基吲唑可使Bcl-2蛋白表达升高，Bax表达降低。提示：局灶性脑缺血再灌注早期，nNOS来源的NO可能通过下调Bcl-2、上调Bax促进细胞凋亡的发生。[著者文摘]
文章出处:
《神经解剖学杂志》-2005年21卷5期 -539-542页
栏目信息:
EFFECTS OF nNOS-DERIVED NO ON Bcl-2 AND Bax PROTEIN EXPRESSION FOLLOWING FOCAL CEREBRAL ISCHEMIA AND REPERFUSION IN RATS
Zhao Yu, Li Li, Yin Qing, Luo bo, Li Chenli, Wang Huijuan, Ma Hongjun （ 1. Department of Histology and Embryology, Hebei Medical University, Shijiazhuang 050017 ; 2 Public Health Centre of Yuhua West Road, Shijiazhuang 050017）
Abstract:
The effects of neuronal nitric oxide synthase （ nNOS）-derived nitric oxide （NO） and peroxynitrite （ ONOO ^- ） on Bel-2 and Bax protein expression were investigated following focal cerebral ischemia and reperfusion in rats. Focal cerebral isehemic model was developed by the occlusion of left middle eerebral artery. 7-nitroindazole, a selective inhibitor of nNOS, was given intraperitoneally. The rats were sacrificed at 6 h of reperfusion after 2 h of ischemia. The Bel-2 and Bax expression were detected immunohistochemically. The expression of Bcl-2 protein was remarkably higher while that of Bax was lower in 50 mg/kg and 25 mg/kg 7-nitroindazole groups than vehicle group. The results indieate that NO derived front nNOS might promote apoptosis in the early stage of cerebral isehemia via upregulating Bax and downregulating Bel-2 expression.[著者文摘]
Key words:
cerebral ischemia, apoptosis, Bcl-2, Bax, nitric oxide, peroxynitrite
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