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机构地区:[1]青岛大学医学院病理生理学教研室,山东青岛266021
出 处:《青岛大学医学院学报》2008年第5期379-381,共3页Acta Academiae Medicinae Qingdao Universitatis
基 金:国家自然科学基金资助项目(30470642);青岛市科技局资助项目(05-1-JC-93)
摘 要:目的观察17β-雌二醇(17β-Ez2)对新生大鼠缺氧缺血性脑损伤(HIBD)模型脑细胞凋亡及血清sFas、sFasL水平的影响。方法将7日龄SD大鼠75只随机分为假手术组、HIBD组以及HIBD+E2组,每组25只。采用双抗体夹心酶联免疫吸附法(ELISA法)分别测定血浆sFas、sFasL的含量,TUNEL法检测脑细胞凋亡率。结果HIBD+E2组与HIBD组相比,CA1区的凋亡细胞数明显减少,尤其在24h最明显;sFas、sFasL水平在各个时间点均明显降低,尤其在48h最明显(F=2.37-21.02,q=2.32-8.34,P〈0.05、0.01)。结论腹腔内给予17β-E2可明显减少HIBD模型鼠海马CA1区细胞凋亡,sFas、sFasL水平呈明显回降。Objective To study the effect of 17β-estradiol on cerebrocellular apoptosis of poxic-ischemic brain damage (HIBD) in neonatal rats, and on serum sFas, sFasL level in brain tissue. Methods Seventy-five 7-day old Wistar rats were even- ly divided into sham-operation, HIBD and HIBD+E2 group. The number of cerebrocellular apoptosis was detected by HE and TUNEL and plasma sFas and sFasL measured by ELISA. Results In the intervention group, the number of apoptotic neurons was much fewer than that in HIBD group (P〈0.01), and concentration of sFas and sFasL was much lower than that in control group, especially in 48 h (P〈0.05,0.01). Conclusion 17β-estradiol could inhibit neuronal apoptosis to protect neurons and attenuated brain injury after HIBD in neonatal rats. And the concentration of sFas and sFasL in the intervention group was lower than that of the control group.
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