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新生大鼠高胆红素血症脑组织Bcl-2表达及干预研究 被引量:2

Research on the Expression and Intervention of Bcl-2 in Brain Tissue of Neonatal Rats with Hyperbilirubinemia
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摘要 目的探讨单唾液酸四己糖神经节苷脂(GM1)对高胆红素血症脑损伤的作用及可能机制。方法将新生7日龄健康SD大鼠120只随机分为对照组、模型组、干预组,各40只。在制作高胆红素血症动物模型基础上予GM1干预,观察3组大鼠脑组织细胞凋亡和Bcl-2表达情况。结果模型组与干预组脑组织均出现凋亡细胞和Bcl-2的表达;对照组未见明显凋亡细胞和Bcl-2的表达。与模型组比较,干预组凋亡细胞和Bcl-2的表达均明显增多,差异有统计学意义(P <0.05)。结论脑细胞凋亡参与高胆红素血症脑损伤的进程。GM1有脑保护作用,其机制可能为通过促进Bcl-2的表达,进而减少细胞凋亡。 Objective To investigate the influence of monosialotetrahexosylganglioside(GM1)on brain injury and its possible mechanism in neonatal rats with hyperbilirubinemia.Methods Sprague Dawley rats(7days old)were randomly divided into three groups(n=40each group)as follows:control group,model group,intervention group.Hyperbilirubinemia newborn rats were set up as animal model.On the basis of setting up animal model,we treated the hyperbilirubinemia newborn rats with GM1and observed the expression of Bcl-2and apoptosis index(AI)in brain tissue of rats,respectively.Results The expression of Bcl-2and AI in model group and intervention group could be detected,whereas no significant expression in control group.The expression of Bcl-2and AI in intervention group was higher than that in the model group(P<0.05).Conclusion Apoptosis of brain cells is involved in the process of hyperbilirubinemia brain damage,GM1has brain protective effect,and its mechanism may be to reduce brain cells apoptosis by promoting the expression of Bcl-2,thereby inhibiting apoptosis.
作者 武师润 阴怀清 李卫卫 白丹 夏莉 杜宜洋 刘榕 朱珊 Wu Shirun;Yin Huaiqing;Li Weiwei;Bai Dan;Xia Li;Du Yiyang;Liu Rong;Zhu Shan(The First Hospital of Shanxi Medical University,Taiyuan 030001,Shanxi,China)
出处 《中西医结合心脑血管病杂志》 2018年第22期3270-3274,共5页 Chinese Journal of Integrative Medicine on Cardio-Cerebrovascular Disease
基金 山西省归国留学人员科研资助项目(No.2014-075)
关键词 高胆红素血症 脑损伤 单唾液酸四己糖神经节苷脂 细胞凋亡 BCL-2 hyperbilirubinemia brain damage monosialotetrahexosylganglioside apoptosis Bcl-2
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