肺气肿小鼠骨骼肌γ谷氨酰半胱氨酸合成酶的表达及意义

The expression of γ-glutamylcysteine synthetase in the skeletal muscles of mice with emphysema and its significance

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.