【摘 要】
：
目的 通过分别抑制大鼠肺泡巨噬细胞(Alveolar macrophage,AM)表面胶原样结构巨噬细胞受体(Macrophage receptor with collagenous structure,MARCO)、AM内活性氧(Reacti
【机 构】
：
新乡医学院公共卫生学院河北联合大学公共卫生学院国家安全生产监督管理总局北戴河职业病防治院
【出 处】
：
中华预防医学会自由基预防学专业委员会2014年学术交流会议
论文部分内容阅读
目的 通过分别抑制大鼠肺泡巨噬细胞(Alveolar macrophage,AM)表面胶原样结构巨噬细胞受体(Macrophage receptor with collagenous structure,MARCO)、AM内活性氧(Reactive oxygen specises,ROS)活性、AM线粒体膜通透性转换孔开放程度以及Caspase-9活性,探讨MARCO、ROS及线粒体凋亡在矽肺发生发展中的作用。材料与方法 无特定病原体级健康成年雄性SD大鼠176只按体重随机分为6组：生理盐水对照组(24只)、矽肺模型组(24只)、N-乙酰半胱氨酸(N-Acetylcysteine,NAC)组(32只)、环孢霉素A(Cyclosporin A,CsA)组(32只)、天冬半胱氨酸特异性蛋白-9(Cysteinyl aspartate specific protease-9,Caspase-9)抑制剂组(32只)、多聚鸟苷酸(Polyguanylic acid,PolyG)组(32只),各组按照施加干预的时间点不同分为预防组和治疗组,预防性及治疗性干预均设置后续观察组(继续观察28天)。
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