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目的观察黄芪甲苷对慢性阻塞性肺疾病(COPD)大鼠内质网应激诱导的肺泡上皮细胞凋亡的保护作用。方法将60只SD大鼠,随机分为对照组、模型组和黄芪甲苷低、中、高剂量组,每组12只;除对照组其余各组均采用气管内滴注脂多糖联合熏烟方法制备COPD大鼠模型,采用原位末端脱氧核苷酸转移酶标记法(TUNEL)法测定各组大鼠肺组织中细胞凋亡情况,采用Western blot法检测各组大鼠肺组织中caspase-3、caspase-12的表达水平。结果与对照组比较,模型组大鼠肺组织中细胞凋亡数量[(173.13±19.20)个/视野]明显升高;与模型组比较,黄芪甲苷高、中、低剂量组大鼠肺组织中细胞凋亡数量[分别为(149.23±8.95)、(118.77±9.47)、(78.87±9.59)个/视野]均减少(P<0.01);与对照组比较,模型组大鼠肺组织中caspase-3、caspase-12表达[分别为(0.847±0.103)、(0.706±0.042)]均升高;与模型组比较,黄芪甲苷高、中、低剂量组大鼠肺组织中caspase-3表达量[分别为(0.412±0.057)、(0.508±0.084)、(0.714±0.061)]与caspase-12表达量[分别为(0.341±0.052)、(0.393±0.065)、(0.516±0.087)]均降低(P<0.01)。结论黄芪甲苷可减轻内质网应激介导的肺组织细胞凋亡,其机制可能与降低大鼠肺组织中凋亡相关蛋白caspase-3、caspase-12表达有关。
Objective To observe the protective effect of astragaloside on apoptosis of alveolar epithelial cells induced by endoplasmic reticulum stress in chronic obstructive pulmonary disease (COPD) rats. Methods Sixty Sprague-Dawley rats were randomly divided into control group, model group and astragaloside low, medium and high dose groups, with 12 rats in each group. Except the control group, the other groups were treated with intratracheal instillation of lipopolysaccharide combined with smoking Methods COPD rat model was established. TUNEL method was used to determine the apoptosis of lung tissue in each group. Western blot was used to detect the expression of caspase- 3, caspase-12 expression levels. Results Compared with the control group, the number of apoptotic cells in the lung tissue of the model group [(173.13 ± 19.20) / visual field] was significantly increased. Compared with the model group, the lung tissue of rats in the high, middle and low dose groups of astragaloside (149.23 ± 8.95), (118.77 ± 9.47) and (78.87 ± 9.59) / visual fields, respectively, compared with the control group (P <0.01). Compared with the control group, the levels of caspase (0.847 ± 0.103) and (0.706 ± 0.042), respectively. Compared with the model group, the expression of caspase-3 in the lung tissue of high, medium and low dose astragaloside group rats (0.412 ± 0.057, 0.508 ± 0.084 and 0.714 ± 0.061, respectively) were significantly correlated with the expression of caspase-12 (0.341 ± 0.052, 0.393 ± 0.065, 0.516 ± 0.087, Decreased (P <0.01). Conclusion Astragaloside can reduce endoplasmic reticulum stress-induced apoptosis of lung cells, which may be related to the decrease of the expression of caspase-3 and caspase-12 in lung tissue of rats.