海马CA1区细胞凋亡.doc

　　　　　 PAGE 6 [收稿日期]: [基金资助]： 辽宁省教育厅计划项目资助2009A462 [作者简介]：袁静，女，学士，主任医师，主要研究方向为危重病性肌病发病机制研究，E-mail: mianyizuhua@ 电话0416-4673682 [通讯作者]：包翠芬　E-mail: mianyizuhua@ 电[通讯地址]:辽宁省锦州市松坡路三段四十号辽宁医学院科学实验中心 邮编:121000 1 地塞米松诱导的危重病性肌病的细胞死亡方式 袁静1梁佳2赵颂2包翠芬2* (1.辽宁医学院附属第一医院神经内科 2辽宁医学院科学实验中心 辽宁 锦州 121000) [摘 要]目的　探讨地塞米松诱导的危重病性肌病的细胞死亡方式。方法　SD大鼠被随机分为正常对照组（A组）和实验组（B组）；B组又分为7d、9d、11d三个亚组（n=10）。B组采用5mg/kg地塞米松连续腹腔注射, 每日1次，A组腹腔注射等量的生理盐水。采用肌功能缺损评分判定肌功能缺损情况。利用免疫组化定性定量检测比目鱼肌Active Caspase-3、PARP、pULK的表达情况。 结果　A组无肌肉功能缺损症状；而7d组大鼠70%出现肌肉功能缺损症状，9d、11d组全部出现明显的肌肉功能缺损症状，以11d组缺损程度最为严重。A、B两组Active Caspase-3、PARP均为阴性表达；A组可见少量pULK阳性表达细胞，B组pULK表达显著增强，以11d组表达最为明显。结论　地塞米松诱导的危重病性肌病中无Active Caspase-3、PARP表达，以pULK表达为主，提示该病以自噬性死亡为主要死亡方式。　 【关键词】地塞米松；危重病性肌病；半胱胺酸蛋白酶蛋白-3；多腺苷二磷酸核糖聚合酶；磷酸化自噬相关蛋白1抗体 【中图分类号】　　 　　【文献标识码】 Cell death mode in critical illness myopathy induced by dexamethasone Yuan Jing1, Liang Jia2, Zhao Song2, Bao Cuifen2* (the First Affiliated Hospital 1, Centre of Scientific Expreiment2, Liaoning Medical college, Jinzhou 121001) [Abstract] Objective To investigate the cell death mode in critical illness myopathy induced by dexamethasone(DX).Methods SD rats were randomly divided into normal control group（group A） and experimental group（group B）.The group B was divided into 7d, 9d, 11d three subgroups ( n = 10 ). The group B used DX 5mg/kg i.p.qd, the group A Injected with equal quality of physiological saline. The clinical scores of Lennon was used to assess the severity of muscle function defect. Immunohistochemistry was used to qualitative and quantitative detect the expression of Caspase3, PARP and pULK in the soleus muscle. Results All rats had no muscle impairment symptoms in group A; whereas 70% rats showed muscle impairment symptoms in 7d experimental group, all rats showed significant muscle impairment in 9d and 11d experimental group, especially in the 11d group. Caspase3 and PARP expression were both negative