辛伐他汀对COPD大鼠肺组织血红素氧化酶-1及炎性因子表达的影响

发布时间：2018-05-28 08:24

本文选题：慢性阻塞性肺疾病 + 吸烟　；参考：《中国老年学杂志》2017年19期

【摘要】：目的探讨辛伐他汀对慢性阻塞性肺疾病(COPD)大鼠肺组织血红素氧化酶(HO)-1表达的影响。方法 24只SD大鼠按随机数字表法分为3组,每组8只。对照组:第1、15天气管内滴入生理盐水0.2 ml,其余时间正常喂养;烟雾暴露组:第1、15天气管内滴入脂多糖0.2 ml,将8只大鼠放进大鼠吸烟装置染毒箱内COPD建模;辛伐他汀组:建立COPD模型方法同上,每次熏烟结束后,给予辛伐他汀灌胃治疗(5 mg/kg),置于相同的环境中喂养。右心导管测定大鼠平均肺动脉压(m PAP),以右心室肥厚指数(RVHI)作为评价右心室肥厚的指标。苏木精-伊红(HE)染色检测大鼠肺组织病理学变化。实时定量PCR(RT-PCR)方法测定肺组织HO-1 mRNA的表达,通过Western印迹及免疫组织化学方法检测肺组织HO-1蛋白的表达。酶联免疫吸附测定法(ELISA)检测支气管肺泡灌洗液(BALF)和血清白细胞介素(IL)-6、肿瘤坏死因子(TNF)-α的水平。结果辛伐他汀组m PAP较烟雾暴露组下降,烟雾暴露组较对照组升高(P0.05)。辛伐他汀组RVHI较烟雾暴露组下降(P0.05)。辛伐他汀组镜下观察气管壁增厚,管腔变窄且肺动脉壁增厚,但是较烟雾暴露组减轻。免疫组织化学实验结果显示,辛伐他汀组肺动脉平滑肌细胞、内皮细胞膜上出现的棕黄色颗粒最多。辛伐他汀组HO-1 mRNA是对照组的(7.26±2.11)倍。烟雾暴露组大鼠HO-1表达增强,辛伐他汀治疗后表达进一步增强。在BALF中,IL-6和TNF-α在辛伐他汀组、烟雾暴露组较对照组表达增加(P0.05)。辛伐他汀组、烟雾暴露组均较对照组血清IL-6表达增加(P0.05),TNF-α在辛伐他汀组、烟雾暴露组较对照组表达增加(P0.05),辛伐他汀组中TNF-α表达量较烟雾暴露组降低(P0.05)。结论辛伐他汀能够促进COPD表达HO-1,减轻COPD炎症反应,改善COPD的发生发展及预后。
[Abstract]:Objective to investigate the effect of simvastatin on the expression of heme oxygenase-1 (HO-1) in rats with chronic obstructive pulmonary disease (COPD). Methods 24 SD rats were randomly divided into 3 groups with 8 rats in each group. In the control group, 0.2 ml of normal saline was dripped into the 1st 15 weather tube, and the rest time was fed normally. In the smoke exposure group, the LPS 0.2 ml was dripped into the 1st 15 weather tube, and the 8 rats were put into the COPD model of the poison box of the smoking device of the rats. Simvastatin group: the COPD model was established in the same way. After each smoking, simvastatin was given intragastric administration of simvastatin for 5 mg / kg and was fed in the same environment. The right ventricular hypertrophy index (RVHI) was used to evaluate the right ventricular hypertrophy. The histopathological changes of rat lung were detected by hematoxylin-eosin-hehe staining. The expression of HO-1 mRNA in lung tissue was detected by real-time quantitative PCR RT-PCR, and the expression of HO-1 protein in lung tissue was detected by Western blot and immunohistochemistry. The levels of BALF6 and TNF- 伪 in bronchoalveolar lavage fluid (bronchoalveolar lavage fluid) and serum interleukin-6 (IL-6) and tumor necrosis factor (TNF- 伪) were detected by enzyme linked immunosorbent assay (Elisa). Results the m PAP of simvastatin group was lower than that of smoke exposure group, and that of smoke exposure group was higher than that of control group. The RVHI of simvastatin group was lower than that of smoke exposure group (P 0.05). In simvastatin group, the wall of trachea was thickened, the lumen narrowed and the pulmonary artery thickened, but it was less severe than that of smoke exposure group. The results of immunohistochemistry showed that in simvastatin group, most brown granules appeared on the endothelial cell membrane of pulmonary artery smooth muscle cells. HO-1 mRNA in simvastatin group was 7.26 卤2.11 times higher than that in control group. The expression of HO-1 was increased in smoke exposure group, and further increased after simvastatin treatment. The expression of IL-6 and TNF- 伪 in BALF in simvastatin group was higher than that in control group (P 0.05). In simvastatin group and smoke exposure group, the expression of serum IL-6 was increased in simvastatin group and smoke exposure group. The expression of TNF- 伪 in simvastatin group was higher than that in control group. The expression of TNF- 伪 in simvastatin group was lower than that in smog exposure group, and the expression of TNF- 伪 in simvastatin group was lower than that in smoke exposure group. Conclusion Simvastatin can promote the expression of HO-1 in COPD, alleviate the inflammatory reaction of COPD, and improve the development and prognosis of COPD.
【作者单位】：锦州医科大学附属第三医院重症医学科;锦州医科大学附属第三医院医学检验中心;
【基金】：辽宁省科学技术计划项目(No.2015020355)
【分类号】：R563.9

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