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机构地区:[1]华中科技大学同济医学院附属协和医院老年科,武汉430022
出 处:《中华物理医学与康复杂志》2012年第7期498-500,共3页Chinese Journal of Physical Medicine and Rehabilitation
摘 要:目的探讨γ谷氨酰半胱氨酸合成酶(γ-GCS)在肺气肿小鼠骨骼肌中的表达变化。方法雄性昆明种小鼠,体重24~26g,按随机数字表法分为正常对照组(10只)和肺气肿组(10只)。肺气肿组采用单纯熏香烟法制作肺气肿小鼠模型(造模成功率80%)。两组均采用TUNEL法检测骨骼肌细胞凋亡情况,采用免疫组化技术检测骨骼肌γ-GCS的蛋白水平变化。结果肺气肿组骨骼肌细胞凋亡平均光密度值(OD)为0.359±0.039,较正常对照组骨骼肌细胞凋亡OD(0.202±0.073)增加(P〈0.05);正常对照组小鼠γ-GCS的蛋白OD水平为0.086±0.008,肺气肿小鼠组γ—GCS的蛋白OD水平为0.210±0.026,两组比较,差异均有统计学意义(P〈0.05)。结论肺气肿小鼠骨骼肌细胞凋亡增加,其机制可能与γ-GCS介导的氧化-抗氧化失衡有关。Objective To study any change in the expression of γ-glutamylcysteine synthetase (γ-GCS) in the skeletal muscles of mice with emphysema. Methods Twenty Kunming male mice were divided into a normal control group and an emphysema group (n = 10 in each). An emphysema model was established by passive cigarette smoking in 8 of the emphysema group mice. TUNEL staining was used to detect apoptotic skeletal muscle cells. Immunohistochemical assays were used to determine the protein level of γ-GCS synthetase. Results The average optical density of apoptotic cells was significantly higher in the skeletal muscles of the mice with emphysema compared with the normal controls, and their average γ-GCS synthetase levels were also significantly higher. Conclusions Apoptotic cells increase in skeletal muscle during emphysema, which may be caused by an oxidation/antioxidant imbalance mediated by γ-GCS synthetase.
关 键 词:肺气肿 慢性阻塞性肺疾病 Γ谷氨酰半胱氨酸合成酶 骨骼肌
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