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目的探讨辛伐他汀对慢性阻塞性肺疾病(COPD)模型大鼠肺组织凋亡相关因子的影响及作用机制。方法随机将30只大鼠分为正常组、对照组、治疗组。对照组采用熏香烟加气管内滴入LPS法建立大鼠COPD模型,香烟暴露2周后治疗组同时给予辛伐他汀(2.5 mg/kg)治疗6周,8周后处死所有大鼠,HE染色观察大鼠肺组织病理改变,显微图像分析系统计算肺平均内衬间隔和平均肺泡数,免疫组织化学技术检测大鼠肺组织半胱氨酸蛋白酶-3(Caspase-3)、诱导型一氧化氮合酶(iNOS)和内皮型一氧化氮合酶(eNOS)的水平。结果对照组可见肺气肿和气道周围炎性改变,治疗组症状较对照组减轻;与正常组相比,对照组和治疗组肺平均内衬间隔(MLI)、iNOS、Caspase-3增多(P<0.05),平均肺泡数(MAN)、eNOS减少(P<0.05);与对照组比较,治疗组MLI、iNOS、Caspase-3减少(P<0.05),MAN、eNOS增多(P<0.05)。各组大鼠肺组织中Caspase-3与iNOS呈正相关(P<0.05),与eNOS呈负相关(P<0.05)。结论辛伐他汀通过增加肺组织eNOS表达,降低iNOS及Caspase-3表达,减少COPD肺组织细胞凋亡,在COPD中起到保护性作用。
Objective To investigate the effects of simvastatin on lung-related apoptosis-related factors in chronic obstructive pulmonary disease (COPD) model rats and its mechanism. Methods Thirty rats were randomly divided into normal group, control group and treatment group. In the control group, the model of COPD was established by the method of cigarette smoking by adding LPS into the trachea and the rats in the treatment group were treated with simvastatin (2.5 mg / kg) for 2 weeks. After 8 weeks, all the rats were sacrificed and the HE staining The pathological changes in the lung tissue of the rats were observed. The average lung lining interval and the average alveolar number were calculated by the microscopic image analysis system. The expressions of caspase-3, Levels of nitric oxide synthase (iNOS) and endothelial nitric oxide synthase (eNOS). Results In the control group, the emphysema and inflammatory changes around the airway were observed. The symptoms in the treatment group were relieved compared with those in the control group. Compared with the normal group, the mean lined intervals (MLI), iNOS and Caspase-3 in the control group and the treatment group increased (P <0.05). The mean alveolar number (MAN) and eNOS decreased (P <0.05). Compared with the control group, the levels of MLI, iNOS and Caspase-3 in the treatment group decreased (P <0.05) and the levels of MAN and eNOS increased (P <0.05). There was a positive correlation between Caspase-3 and iNOS (P <0.05), but negative correlation with eNOS (P <0.05). Conclusion Simvastatin can play a protective role in COPD by increasing the expression of eNOS in lung tissue, decreasing the expression of iNOS and Caspase-3, and decreasing the apoptosis of COPD lung tissue.